| 1. |
- Ainegren, Mats, 1963-, et al.
(författare)
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Breathing resistance in heat and moisture exchanging devices
- 2022
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Ingår i: Proceedings of the Institution of Mechanical Engineers, Part P. - : Sage Publications. - 1754-3371. ; 236:2, s. 97-105
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the resistance to breathing (RES) in heat and moisture exchanging devices (HME) intended for use during physical activity in the cold. RES was investigated for seventeen HMEs, including different types of filters. In addition, the influence of headwind on RES was tested using four representative HMEs. HMEs were mounted to the face of an artificial head manufactured from ABS plastic. The HMEs were connected to a mechanical lung simulator, which delivered standardised inspiratory and expiratory air flow rates (V⋅, L/s). The delta pressure (Δp, Pa) between ambient air and the air inside the HME was measured, whereupon RES was calculated. The results showed significant (p < 0.05) differences in RES between HMEs from different manufacturers, while the difference was smaller, and in some cases not significant (p > 0.05), between different models/filters within the same brand. The results also showed that RES was highly influenced by different ventilations and headwind conditions. RES increased with increased V⋅ and, when a headwind was introduced, RES decreased during inspiration and increased during expiration. Calculations showed that the oxygen and energy cost for breathing through an HME was very small for most of the tested models. The effect of HME dead space on pulmonary gas fractions depends on the tidal volume. At large tidal volumes and ventilations, the effect of HMEs on pulmonary gas fractions becomes relatively small.
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| 2. |
- Andreassen, Siw Lillevik, et al.
(författare)
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Impact of pneumonia on hospitalizations due to acute exacerbations of COPD
- 2014
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Ingår i: Clinical Respiratory Journal. - : Wiley. - 1752-6981 .- 1752-699X. ; 8:1, s. 93-99
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Pneumonia is often diagnosed among patients hospitalized with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The aims of this study were to find the proportion of patients with pneumonia among admissions due to AECOPD and whether pneumonia has impact on the length of stay (LOS), usage of non-invasive ventilation (NIV) or the in-hospital mortality.METHODS: Retrospectively, all hospitalizations in 2005 due to AECOPD in the Departments of Internal and Respiratory Medicine in one Swedish and two Norwegian hospitals were analyzed. A total of 1144 admittances (731 patients) were identified from patient administrative systems. Pneumonic AECOPD (pAECOPD) was defined as pneumonic infiltrates on chest X-ray and C-reactive protein (CRP) value of ≥40 mg/L, and non-pneumonic AECOPD (npAECOPD) was defined as no pneumonic infiltrate on X-ray and CRP value of <40 at admittance.RESULTS: In admissions with pAECOPD (n = 237), LOS was increased (median 9 days vs 5 days, P < 0.001) and usage of NIV was more frequent (18.1% vs 12.5%, P = 0.04), but no significant increase in the in-hospital mortality (3.8% vs 3.6%) was found compared to admissions with npAECOPD. A higher proportion of those with COPD GOLD stage I-II had pAECOPD compared to those with COPD GOLD stage III-IV (28.2% vs 18.7%, P = 0.001).CONCLUSIONS: In-hospital morbidity, but not mortality, was increased among admissions with pAECOPD compared to npAECOPD. This may, in part, be explained by the extensive treatment with antibiotics and NIV in patients with pAECOPD.
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| 3. |
- Backman, Helena, et al.
(författare)
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All-cause and cause-specific mortality by spirometric pattern and sex - a population-based cohort study
- 2024
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Ingår i: THERAPEUTIC ADVANCES IN RESPIRATORY DISEASE. - : Sage Publications. - 1753-4658 .- 1753-4666. ; 18
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Tidskriftsartikel (refereegranskat)abstract
- Background: Chronic airway obstruction (CAO) and restrictive spirometry pattern (RSP) are associated with mortality, but sex-specific patterns of all-cause and specific causes of death have hardly been evaluated. Objectives: To study the possible sex-dependent differences of all-cause mortality and patterns of cause-specific mortality among men and women with CAO and RSP, respectively, to that of normal lung function (NLF). Design: Population-based prospective cohort study. Methods: Individuals with CAO [FEV1/vital capacity (VC) < 0.70], RSP [FEV1/VC >= 0.70 and forced vital capacity (FVC) < 80% predicted] and NLF (FEV1/VC >= 0.70 and FVC >= 80% predicted) were identified within the Obstructive Lung Disease in Northern Sweden (OLIN) studies in 2002-2004. Mortality data were collected through April 2016, totally covering 19,000 patient-years. Cox regression and Fine-Gray regression accounting for competing risks were utilized to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) adjusted for age, body mass index, sex, smoking habits and pack-years. Results: The adjusted hazard for all-cause mortality was higher in CAO and RSP than in NLF (HR, 95% CI; 1.69, 1.31-2.02 and 1.24, 1.06-1.71), and the higher hazards were driven by males. CAO had a higher hazard of respiratory and cardiovascular death than NLF (2.68, 1.05-6.82 and 1.40, 1.04-1.90). The hazard of respiratory death was significant in women (3.41, 1.05-11.07) while the hazard of cardiovascular death was significant in men (1.49, 1.01-2.22). In RSP, the higher hazard for respiratory death remained after adjustment (2.68, 1.05-6.82) but not for cardiovascular death (1.11, 0.74-1.66), with a similar pattern in both sexes. Conclusion: The higher hazard for all-cause mortality in CAO and RSP than in NLF was male driven. CAO was associated with respiratory death in women and cardiovascular death in men, while RSP is associated with respiratory death, similarly in both sexes.
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| 4. |
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| 5. |
- Behndig, Annelie, et al.
(författare)
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Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.
- 2006
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 27:2, s. 359-365
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Tidskriftsartikel (refereegranskat)abstract
- Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly. A total of 15 volunteers were exposed to DE (100 microg x m(-3) airborne particulate matter with a diameter of <10 microm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status. Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure. In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.
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| 6. |
- Behndig, Annelie F., et al.
(författare)
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Effects of controlled diesel exhaust exposure on apoptosis and proliferation markers in bronchial epithelium : an in vivo bronchoscopy study on asthmatics, rhinitics and healthy subjects
- 2015
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Ingår i: BMC Pulmonary Medicine. - : Springer Science and Business Media LLC. - 1471-2466. ; 15
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Tidskriftsartikel (refereegranskat)abstract
- Background: Epidemiological evidence demonstrates that exposure to traffic-derived pollution worsens respiratory symptoms in asthmatics, but controlled human exposure studies have failed to provide a mechanism for this effect. Here we investigated whether diesel exhaust (DE) would induce apoptosis or proliferation in the bronchial epithelium in vivo and thus contribute to respiratory symptoms.Methods: Moderate (n = 16) and mild (n = 16) asthmatics, atopic non-asthmatic controls (rhinitics) (n = 13) and healthy controls (n = 21) were exposed to filtered air or DE (100 μg/m 3 ) for 2 h, on two separate occasions. Bronchial biopsies were taken 18 h post-exposure and immunohistochemically analysed for pro-apoptotic and anti-apoptotic proteins (Bad, Bak, p85 PARP, Fas, Bcl-2) and a marker of proliferation (Ki67). Positive staining was assessed within the epithelium using computerized image analysis.Results: No evidence of epithelial apoptosis or proliferation was observed in healthy, allergic or asthmatic airways following DE challenge.Conclusion: In the present study, we investigated whether DE exposure would affect markers of proliferation and apoptosis in the bronchial epithelium of asthmatics, rhinitics and healthy controls, providing a mechanistic basis for the reported increased airway sensitivity in asthmatics to air pollutants. In this first in vivo exposure investigation, we found no evidence of diesel exhaust-induced effects on these processes in the subject groups investigated.
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| 7. |
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| 8. |
- Bolger, Claire, et al.
(författare)
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Urinary cc16 levels in winter versus summer sport athletes after eucapnic voluntary hyperpnoea
- 2009
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Konferensbidrag (refereegranskat)abstract
- Exercise induced bronchoconstriction (EIB) is highly prevalent in elite athletes, especially in those training in cold dry environments. Dehydration of the airways plays a key role in this process. EIB has recently been linked to airway epithelial injury in asthmatic individuals. The aim of the study is to determine whether a short period of hyperpnoea of dry air causes airway epithelial disruption in winter and/or summer sport athletes. We hypothesise that urinary level of the Clara cell protein (CC16) – an indirect marker of permeability/cellular integrity of the lung epithelial barrier – will be increased after a eucapnic voluntary hyperpnoea (EVH) test and that this increase will be larger in winter compared to summer athletes. Forty two female athletes – 28 summer athletes (age 31.1+/-1.7yr (SEM), training volume 9+/-1.1h/wk) and 14 winter athletes (age 21.4+/-0.8yr, training volume 12.0 ± 1.10h/wk) – took part in this study. They all performed an 8-min EVH test at a target ventilation rate of 30 times their baseline forced expiratory volume in one second (FEV1). After the challenge, FEV1 was measured in duplicate at 2, 5, 10, 15, 20, 30, 60 and 90min. A sustained decrease in FEV1 of at least 10% from baseline was considered positive. Urine samples were collected at baseline and at 30, 60 and 90min recovery. CC16 concentration was measured by enzyme immunoassay. Ten summer athletes had a positive test (max FEV1 fall = 19.6+/-2.4%), whilst eighteen of the summer athletes and all the winter athletes were negative (max FEV1 fall = 5.7+/-0.7% and 5.3+/-0.7%, respectively). CC16 increased significantly after the challenge in all three groups (P<0.01) with no difference between groups: delta CC16 (max post-EVH minus baseline) in summer EVH negative athletes was 0.241+/-0.1 ng/μmol creatinine, 0.292+/-0.085 ng/μmol creatinine in summer EVH positive athletes, and 0.123+/-0.047ng/μmol creatinine in winter EVH negative athletes (P=0.415)In conclusion, a short period of hyperpnoea of dry air is associated with an increased rate of CC16 excretion in urine in both winter and summer athletes. This suggests that the integrity of the airway epithelium might be compromised by loss of airway surface lining fluid when athletes inhale dry air at high flow rates. This appears to occur irrespective of the degree of bronchoconstriction or regular training environment.
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| 9. |
- Bosson, Jenny A, et al.
(författare)
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Peripheral blood neutrophilia as a biomarker of ozone-induced pulmonary inflammation
- 2013
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 8:12
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Ozone concentrations are predicted to increase over the next 50 years due to global warming and the increased release of precursor chemicals. It is therefore urgent that good, reliable biomarkers are available to quantify the toxicity of this pollutant gas at the population level. Such a biomarker would need to be easily performed, reproducible, economically viable, and reflective of ongoing pathological processes occurring within the lung.METHODOLOGY: We examined whether blood neutrophilia occurred following a controlled ozone challenge and addressed whether this could serve as a biomarker for ozone-induced airway inflammation. Three separate groups of healthy subjects were exposed to ozone (0.2 ppm, 2h) and filtered air (FA) on two separate occasions. Peripheral blood samples were collected and bronchoscopy with biopsy sampling and lavages was performed at 1.5h post exposures in group 1 (n=13), at 6h in group 2 (n=15) and at 18h in group 3 (n=15). Total and differential cell counts were assessed in blood, bronchial tissue and airway lavages.RESULTS: In peripheral blood, we observed fewer neutrophils 1.5h after ozone compared with the parallel air exposure (-1.1±1.0x10(9) cells/L, p<0.01), at 6h neutrophil numbers were increased compared to FA (+1.2±1.3x10(9) cells/L, p<0.01), and at 18h this response had fully attenuated. Ozone induced a peak in neutrophil numbers at 6h post exposure in all compartments examined, with a positive correlation between the response in blood and bronchial biopsies.CONCLUSIONS: These data demonstrate a systemic neutrophilia in healthy subjects following an acute ozone exposure, which mirrors the inflammatory response in the lung mucosa and lumen. This relationship suggests that blood neutrophilia could be used as a relatively simple functional biomarker for the effect of ozone on the lung.
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| 10. |
- Bosson, Jenny, et al.
(författare)
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Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects
- 2003
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Ingår i: Clinical and Experimental Allergy. - : Wiley. - 0954-7894 .- 1365-2222. ; 33:6, s. 777-782
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Tidskriftsartikel (refereegranskat)abstract
- Background Ozone (O3) is a common air pollutant associated with adverse health effects. Asthmatics have been suggested to be a particularly sensitive group. Objective This study evaluated whether bronchial epithelial cytokine expression would differ between healthy and allergic asthmatics after ozone exposure, representing an explanatory model for differences in susceptibility. Methods Healthy and mild allergic asthmatic subjects (using only inhaled β2-agonists prn) were exposed for 2 h in blinded and randomized sequence to 0.2 ppm of O3 and filtered air. Bronchoscopy with bronchial mucosal biopsies was performed 6 h after exposure. Biopsies were embedded in GMA and stained with mAbs for epithelial expression of IL-4, IL-5, IL-6, IL-8, IL-10, TNF-α, GRO-α, granulocyte–macrophage colony-stimulating factor (GM–CSF), fractalkine and ENA-78. Results When comparing the two groups at baseline, the asthmatic subjects showed a significantly higher expression of IL-4 and IL-5. After O3 exposure the epithelial expression of IL-5, GM–CSF, ENA-78 and IL-8 increased significantly in asthmatics, as compared to healthy subjects. Conclusion The present study confirms a difference in epithelial cytokine expression between mild atopic asthmatics and healthy controls, as well as a differential epithelial cytokine response to O3. This O3-induced upregulation of T helper type 2 (Th2)-related cytokines and neutrophil chemoattractants shown in the asthmatic group may contribute to a subsequent worsening of the airway inflammation, and help to explain their differential sensitivity to O3 pollution episodes.
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