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  • 201. Mudway, Ian S
    et al.
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Duggan, Sean T
    Roxborough, Heather
    Zielinski, Hendrick
    Marklund, Stephan L
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Frew, Anthony J
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Kelly, Frank J
    An in vitro and in vivo investigation of the effects of diesel exhaust on human airway lining fluid antioxidants.2004In: Arch Biochem Biophys, ISSN 0003-9861, Vol. 423, no 1, p. 200-12Article in journal (Refereed)
  • 202. Neuman, Asa
    et al.
    Gunnbjörnsdottir, María
    Tunsäter, Alf
    Nyström, Lennarth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Franklin, Karl A
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Norrman, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Janson, Christer
    Dyspnea in relation to symptoms of anxiety and depression: A prospective population study.2006In: Respir Med, ISSN 0954-6111, Vol. 100, no 10, p. 1843-9Article in journal (Refereed)
  • 203.
    Nilsson, Kenneth
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Radiation induced pneumonitis: clinical and experimental studies with special emphasis on the effect of smoking1992Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Bronchoalveolar lavage (BAL) is an established method providing diagnostic support and evaluation of disease activity in interstitial lung disease (ILD). The aims of the present investigation were 1) to study the inflammatory response in pneumonitis evoked by irradiation. 2) to evaluate how well lung tissue inflammation is reflected in BAL findings. 3) to study the effect of smoking on radiation-induced pneumonitis.

    BAL was performed in 21 patients (11 smokers, 10 non-smokers) who were treated for breast cancer, stage 1 (TjMaNq) by post-surgery irradiation to an accumulated target dose of 56 Gy. It was founa that irradiation induced an alveolitis in the non-smoking patient group while the smoking patients did not differ from their smoking controls. The alveolitis in non-smokers was characterized by an increase in lymphocytes, mast cells and elevated concentrations of hyaluronan (HA), and fibronectin (FN). Three of the non-smoking patients had chest X-ray infiltrates indicating the presence of pneumonitis.

    An animal experimental model for radiation-induced pneumonitis and fibrosis was established in rats, allowing comparative analysis of BAL fluid and morphology. In the rat model a divergence was noted between the differential cell counts in BAL and cells observed in the interstitial tissue, which was most notable for neutrophils (PMN) and mast cells whereas there was a good correlation between HA content in BAL and HA deposition in the lung tissue. A marked infiltration of intraseptally-located mast cells occurred during the pneumonitis-phase, and this increase was paralleled by a deposition of HA in the interstitial tissue. Histochemical fixation and staining properties of the mast cells revealed that the majority of these cells were of connective tissue mast cell type (CTMC). Compound 48/80, a mast cell secretagogue, significantly altered the HA content both in BAL and in lung tissue in the irradiated animals. Regular treatment throughout the whole experimental period induced depletion of mast cell granules and a decrease in HA deposition whereas 48/80 treatment during the pneumonitis phase enhanced HA deposition.

    A rat model with smoke exposure was developed, and the effect of cigarette smoke on radiation-induced inflammation was studied. Rats that smoked 3 weeks prior to irradiation and continued to smoke throughout the observation period (7 weeks) had a significantly reduced inflammatory response compared to irradiated non-smoking rats. The most prominent BAL findings in the smoke-exposed rats were a decrease in PMN, mast cells and a decrease in HA.

    In conclusion, irradiation induces an alveolitis characterized mainly by mononuclear cells. Mast cells seem to be of importance in the remodelling of the connective tissue in the radiation-induced inflammatory response. Hyaluronan is an important component in the early connective tissue response preceding later collagen deposition, and its interstitial deposition is very well reflected in BAL. Moreover, tobacco-smoke suppresses the radiation-induced inflammation with a decreased recruitment of effector cells including mast cells.

  • 204.
    Nilsson, Ulf
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johansson, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Eriksson, Berne
    Göteborgs Universitet.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundbäck, Bo
    Göteborgs Universitet.
    Lindberg, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ischemic heart disease among subjects with and without chronic obstructive pulmonary disease: ECG-findings in a population-based cohort study2015In: BMC Pulmonary Medicine, ISSN 1471-2466, E-ISSN 1471-2466, Vol. 15, article id 156Article in journal (Refereed)
    Abstract [en]

    Background: Cardiovascular comorbidity in COPD is common and contributes to increased mortality. A few population-based studies indicate that ischemic electrocardiogram (ECG)-changes are more prevalent in COPD, while others do not.

    The aim of the present study was to estimate the presence of ischemic heart disease (IHD) in a population-based COPD-cohort in comparison with subjects without COPD.

    Methods: All subjects with obstructive lung function (COPD, n = 993) were identified together with age- and sex-matched controls (non-COPD, n = 993) from population-based cohorts examined in 2002–04. In 2005, data from structured interview, spirometry and ECG were collected from 1625 subjects. COPD was classified into GOLD 1–4 after post-bronchodilator spirometry. Ischemic ECG-changes, based on Minnesota-coding, were classified according to the Whitehall criteria into probable and possible IHD.

    Results: Self-reported IHD was equally common in COPD and non-COPD, and so were probable and possible ischemic ECG-changes according to Whitehall. After excluding subjects with restrictive spirometric pattern from the non-COPD-group, similar comparison with regard to presence of IHD performed between those with COPD and those with normal lung-function did neither show any differences. There was a significant association between self-reported IHD (p = 0.007) as well as probable ischemic ECG-changes (p = 0.042), and increasing GOLD stage. In COPD there was a significant association between level of FEV1 percent of predicted and self-reported as well as probable ischemic ECG-changes, and this association persisted for self-reported IHD also after adjustment for sex and age.

    Conclusion: In this population-based study, self-reported IHD and probable ischemic ECG-changes were associated with COPD disease severity assessed by spirometry.

  • 205.
    Nordberg, Gunnar F
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lundström, Nils-Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hagenbjörk-Gustafsson, Annika
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lagerkvist, Birgitta J-Son
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nilsson, Johan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Svensson, Mona
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Nilsson, Leif
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Umeå University, Faculty of Science and Technology, Department of Mathematics and Mathematical Statistics.
    Bernard, Alfred
    Dumont, Xavier
    Bertilsson, Helen
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Eriksson, Kåre
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lung function in volunteers before and after exposure to trichloramine in indoor pool environments and asthma in a cohort of pool workers2012In: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 2, no 5, p. e000973-Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Exposure to trichloramine (NCl(3)) in indoor swimming-pool environments is known to cause mucous membrane irritation, but if it gives rise to changes in lung function or asthma in adults is not known. (1) We determined lung function in volunteers before and after exposure to indoor pool environments. (2) We studied the occurrence of respiratory symptoms and asthma in a cohort of pool workers.

    DESIGN/METHODS/PARTICIPANTS: (1) We studied two groups of volunteers, 37 previously non-exposed healthy persons and 14 pool workers, who performed exercise for 2 h in an indoor pool environment. NCl(3) in air was measured during pool exposures and in 10 other pool environments. Filtered air exposures were used as controls. Lung function and biomarkers of pulmonary epithelial integrity were measured before and after exposure. (2) We mailed a questionnaire to 1741 persons who indicated in the Swedish census 1990 that they worked at indoor swimming-pools.

    RESULTS: (1) In previously non-exposed volunteers, statistically significant decreases in FEV(1) (forced expiratory volume) and FEV(%) (p=0.01 and 0.05, respectively) were found after exposure to pool air (0.23 mg/m(3) of NCl(3)). In pool workers, a statistically significant decrease in FEV(%) (p=0.003) was seen (but no significant change of FEV(1))(.) In the 10 other pool environments the median NCl(3) concentration was 0.18 mg/m(3). (2) Our nested case/control study in pool workers found an OR for asthma of 2.31 (95% CI 0.79 to 6.74) among those with the highest exposure. Exposure-related acute mucous membrane and respiratory symptoms were also found.

    CONCLUSIONS: This is the first study in adults showing statistically significant decreases in lung function after exposure to NCl(3). An increased OR for asthma among highly exposed pool workers did not reach statistical significance, but the combined evidence supports the notion that current workroom exposures may contribute to asthma development. Further research on sensitive groups is warranted.

  • 206.
    Nordenhäll, C
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ledin, M-C
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Levin, Jan-Olof
    Institute for Working Life, Dept of Occupational Chemistry, Umeå.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Diesel exhaust enhances airway responsiveness in asthmatic subjects2001In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 17, no 5, p. 909-915Article in journal (Refereed)
    Abstract [en]

    Particulate matter (PM) pollution has been associated with negative health effects, including exacerbations of asthma following exposure to PM peaks. The aim of the present study was to investigate the effects of short-term exposure to diesel exhaust (DE) in asthmatics, by specifically addressing the effects on airway hyperresponsiveness, lung function and airway inflammation. Fourteen nonsmoking, atopic asthmatics with stable disease, on continuous treatment with inhaled corticosteroids, were included. All were hyperresponsive to methacholine. Each subject was exposed to DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 300 microg x m(-3)) and air during 1 h on two separate occasions. Lung function was measured before and immediately after the exposures. Sputum induction was performed 6 h, and methacholine inhalation test 24 h, after each exposure. Exposure to DE was associated with a significant increase in the degree of hyperresponsiveness, as compared to after air, of 0.97 doubling concentrations at 24 h after exposure (p < 0.001). DE also induced a significant increase in airway resistance (p=0.004) and in sputum levels of interleukin (IL)-6 (p=0.048). No changes were detected in sputum levels of methyl-histamine, eosinophil cationic protein, myeloperoxidase and IL-8. This study indicated that short-term exposure to diesel exhaust, equal to high ambient levels of particulate matter, is associated with adverse effects in asthmatic airways, even in the presence of inhaled corticosteroid therapy. The increase in airway responsiveness may provide an important link to epidemiological findings of exacerbations of asthma following exposure to particulate matter.

  • 207.
    Nordenhäll, Charlotta
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Airway effects of diesel exhaust in healthy and asthmatic subjects2002Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Several epidemiological studies have revealed an association between particulate matter (PM) pollution and various health effects. Importantly, there is evidence to suggest that individuals with pre-existing respiratory disease, such as asthma, are more sensitive to elevated ground levels of particulate matter as compared to healthy subjects. Among the various sources of PM pollution, diesel powered vehicles have been identified as important contributors.

    The aim of this thesis was to investigate the airway effects of experimental chamber exposure to diesel exhaust (DE) in healthy and asthmatic subjects, focusing on airway responsiveness, airway inflammation and lung function. To achieve a comprehensive picture of the airway responses to DE, a number of different methods were used, including lung function measurements, methacholine inhalation tests, induced sputum and bronchoscopy. Each subject acted as his/her own control by being exposed both to filtered air and DE in a crossover design.

    Short term exposure to DE, at a particle concentration (PMi0) of 300 ug/m3, was associated with a clinically significant increase in bronchial hyperresponsiveness in asthmatic subjects. In accordance with the epidemiological data suggesting a 1-4 day lag effect for most health outcomes to PM pollution, the increase was detected one day after DE exposure, indicating a long lasting response to DE in asthmatic airways.

    Diesel exhaust induced a range of airway inflammatory changes as reflected in induced sputum, bronchoalveolar lavage and bronchial mucosal biopsies. In healthy subjects, DE exposure was associated with an increase in neutrophils and IL-6 in sputum, elevated levels of IL-8 and IL-6 in bronchial wash (BW), enhanced expression of IL-8 and GRO-a in the bronchial epithelium and with increases in P-selectin and VCAM-1 in the airway mucosa. In contrast, asthmatics responded with an increase in IL-6 in sputum and an enhanced expression of IL-10 in the bronchial epithelium following exposure DE. Thus, clear differences were identified between healthy and asthmatic subjects in the inflammatory response to DE.

    Airway epithelial cells constitute the first line of cellular defence towards inhaled air pollutants and increasing evidence suggests that these cells contribute markedly to the initiation of airway inflammatory responses. The bronchial epithelium was identified to have an important regulatory role in response to diesel exhaust, including the capacity to produce chemoattractant and immunoregulatory proteins associated with development of airway inflammation and bronchial hyperresponsiveness.

    Lung function measurements revealed that short-term exposure to DE induces an immediate bronchoconstrictive response in both healthy and asthmatic individuals, with significant increases in airway resistance (Raw) following DE exposure.

    This thesis also investigated the effects of a lower concentration of DE (PMio 100 ug/m3) than previously studied. It was shown that exposure to DE at a concentration corresponding to a PM level that may be encountered in busy traffic situations, was still associated with potentially adverse airway responses in healthy and asthmatic subjects.

    In summary, the results presented here indicate that short term exposure to diesel exhaust, at high ambient concentrations, has the potential to induce a range of biological events in the airways of healthy and asthmatic subjects.

  • 208. Norqvist, Johan
    et al.
    Eriksson, Linda
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Söderström, Lars
    Unit of Research , Education and Development - Östersund, Umeå University.
    Lindberg, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Unit of Research , Education and Development - Sunderbyn, Umeå University.
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Unit of Research , Education and Development - Östersund, Umeå University.
    Self-reported physician-diagnosed asthma among Swedish adolescent, adult and former elite endurance athletes2015In: Journal of Asthma, ISSN 0277-0903, E-ISSN 1532-4303, Vol. 52, no 10Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Asthma is common among elite endurance athletes. Since the first published Swedish studies in 1993, awareness of "skiers' asthma" has increased. The current prevalence of asthma among Swedish skiers is unknown. This paper aims to present the design of a 5-year prospective annual questionnaire study on asthma among Swedish current and former elite endurance athletes, the first cross-sectional results on prevalence, age of onset, and predictors of self-reported physician-diagnosed asthma in the study population.

    METHODS: An annual postal questionnaire is sent to Swedish elite skiers and orienteers during 2011-2015. In 2013, former Swedish Olympic skiers were similarly invited. We present cross-sectional data obtained in 2011 from the adolescents and adults and in 2013 from former skiers. A total of 491 athletes were invited. The results are presented by age, sex and sport. Chi-square test was used for group comparisons. Predictors of asthma were identified using logistic regression.

    RESULTS: Response rate was 82%. Among athletes aged 15-19, 29% of the skiers (38% of the female skiers), and 17% of the orienteers reported asthma (p = 0.071). Among the athletes aged 20-34, 35% of the skiers and 16% of the orienteers reported asthma (p = 0.029). Among the former skiers aged 40-94, 22% reported asthma. Among the active athletes, the onset of asthma was in early adolescence. Logistic regression found increasing age, female sex, allergy, family history of allergy/asthma and being skier predictors of self-reported physician-diagnosed asthma.

    CONCLUSIONS: The prevalence of physician-diagnosed asthma is high among Swedish endurance athletes, especially female adolescent skiers.

  • 209.
    Nyström, Robin
    et al.
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pagels, Joakim
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Evaluation of a novel chamber setup for human exposures of biomass combustion aerosolsManuscript (preprint) (Other academic)
    Abstract [en]

    Based on a vast number of epidemiological studies there is today a consensus that increased concentrations of ambient particulate matter air pollution cause adverse health effects such as mortality, hospitalizations, cardiovascular events, respiratory symptoms and reduced lung function. The use of controlled laboratory studies with human exposure chambers can give unique opportunities to directly examine specific exposure conditions and cause-effect relationship with relevant concentrations and particle types. In this paper, the design of a novel chamber setup for human exposures of biomass combustion aerosols is described with an evaluation of the systems function under different conditions (e.g. air exchange rates and target PM1 concentrations). Several different research biomass combustion systems are available in combination with extensive and advanced monitoring and characterization of the gaseous and particle emissions used for exposures. Examples, with data from three performed human exposure campaigns, are included and discussed as a basis for the evaluation of the whole setup, with the target to generate stable conditions in the chamber using different kinds of biomass combustion aerosols. Based on the evaluation of function and present exposure experiences it can be concluded that the chamber setup and biomass aerosol generation systems is able to produce a stable aerosol concentration in the chamber of different particle types.  Overall, the human exposure setup for biomass combustion aerosols together with the integrated biomass combustion laboratory gives extensive possibilities for designing different whole body human exposure studies for a variety of biomass combustion aerosols as well as other experimental aerosol research.

  • 210.
    Nyström, Robin
    et al.
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Nordin, EZ
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    A novel set-up for source characterization and human exposures of biomass combustion aerosols2013Conference paper (Other academic)
  • 211.
    Nyström, Robin
    et al.
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Pagels, Joakim
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Effects of dilution conditions on particle formation and size distribution in engine exhaust emissions when introducing biodiesel in comparison to standard petro dieselManuscript (preprint) (Other academic)
    Abstract [en]

    Air pollution, in particular ambient particulate matter (PM), can be linked to a variety of different health effects, and a major contributor to the PM pollution is exhaust from diesel engines and other vehicles. In the global drive towards finding sustainable and clean bio-based alternative fuels for the transport sector, biodiesel is one of the most established alternative. However, there is considerable variation in emission data for biodiesel, preferably explained by influences of engine technology and operating conditions as well as dilution sampling strategy. In this study the focus was therefore to study the effects of dilution conditions on the particle formation and size distribution in the exhaust emissions from an off road engine, when introducing RME biodiesel in comparison to standard petro diesel. Particle size distribution and number concentration were measured on-line with the use of a fast mobility spectrometer, during a transient operation and without engine modification. Differences in particle characteristics were elucidated in the raw exhaust versus diluted exhaust at two subsequent sampling points with different dilution ratios. In addition, the influences on the exhaust particle properties of changing the lubrication oil was investigated. It was found that biodiesel in general generated more nucleation mode particles then petro diesel, and after the oil exchange the total particle number concentration was increased even more. It was also seen that the custom-built dilution setup favors generation of nucleation mode particles, which is in line with real life conditions in chase and road side experiments. However, when using heated primary dilution and a heated line in the raw exhaust the formation of nucleation mode particles was suppressed. Overall, it was concluded that the introduction of the biodiesel, and potentially other renewable fuels, can in a considerable way change the exhaust particle emission and characteristics. This could have implications for the assessment of exhaust from engines running on biodiesel fuels, especially when introducing biodiesel in existing and older engines.

  • 212.
    Nyström, Robin
    et al.
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Sadiktsis, Ioannis
    Ahmed, Trifa M.
    Westerholm, Roger
    Koegler, Johannes H.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Physical and chemical properties of RME biodiesel exhaust particles without engine modifications2016In: Fuel, ISSN 0016-2361, E-ISSN 1873-7153, Vol. 186, p. 261-269Article in journal (Refereed)
    Abstract [en]

    A major contributor to ambient particulate air pollution is exhaust from diesel engines and other vehicles, which can be linked to different adverse health effects. During the last decades, a global drive towards finding sustainable and clean bio-based alternative fuels for the transport sector has taken place and biodiesel is one of the most established alternatives today. To better assess the overall effects on a public health level when introducing biodiesel and other renewable fuels, a better understanding of the detailed exhaust particle properties, is needed. In this work, the physical and chemical properties of biodiesel exhaust particles were studied in comparison to standard diesel exhaust emissions, in an existing engine without modifications, focusing on particulate carbonaceous matter and PAH/Oxy-PAH as well as fine particle size distribution. An older off-road engine, produced between 1996 and 2004, was used with three different fuels/fuel blends; (1) 100 wt% low-sulfur standard petro diesel (SD), (2) 100 wt% rapeseed methyl ester biodiesel (B100) and (3) a blended fuel – B30 consisting of 30 wt% RME and 70 wt% SD. The study focused mainly on emissions from transient engine operation, but includes also idling conditions. The gaseous emissions measured for the biodiesel fuel were in general in accordance with previous reported data in the literature, and compared to the standard petro diesel the emissions of CO was lower while NOx emissions increased. The particulate mass concentration during transient operation was almost halved compared to when petro diesel was used and this was associated with a decrease in average particle size. The shift in particle mass and size was associated with a higher fraction of organic matter in general, considerable less PAH’s but a relative higher fraction of Oxy-PAH’s, when shifting from petro diesel to biodiesel.

  • 213.
    Nyström, Robin
    et al.
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Sadiktsis, Ioannis
    ept. of Analytical Chemistry, Arrhenius Laboratory, Stockholm University.
    Trifa, Mohammad Ahmed
    Dept. of Analytical Chemistry, Arrhenius Laboratory, Stockholm University.
    Roger, Westerholm
    ept. of Analytical Chemistry, Arrhenius Laboratory, Stockholm University.
    Koegler, Jan
    Volvo Group Trucks Technology, ATR, Gothenburg, Sweden.
    Mudway, Ian S
    4MRC-PHE Centre for Environment and Health, School of Biomedical Sciences, King’s College London, UK.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Properties of biodiesel exhaust particles from two non-road engines2014Conference paper (Other academic)
  • 214.
    Näsman, Amanda
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Irewall, Tommie
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Hållmarker, Ulf
    Lindberg, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Asthma and Asthma Medication Are Common among Recreational Athletes Participating in Endurance Sport Competitions2018In: Canadian Respiratory Journal, ISSN 1198-2241, Vol. 2018, article id 3238546Article in journal (Refereed)
    Abstract [en]

    Background: Asthma prevalence is high among elite endurance athletes, but little is known about its prevalence among competitive recreational athletes. The aim of this study was to determine the prevalence of self-reported asthma and asthma medication use among competitive recreational endurance athletes and their association with training.

    Methods: A web survey on asthma and medication was conducted among 38,603 adult participants of three Swedish endurance competitions (cross-country running, cross-country skiing, and swimming).

    Results: The overall response rate was 29%. The prevalence of self-reported asthma (physician-diagnosed asthma and use of asthma medication in the last 12 months) was 12%. Among those reporting asthma, 23% used inhaled corticosteroids and long-acting beta-agonists daily. We found no association between training volume and daily use of asthma medication, except a trend in relation to short-acting beta-agonists. Independent predictors of self-reported asthma were female sex, allergic rhinitis, previous eczema, family history of asthma, cycling, and training for >5 h 50 min/week.

    Conclusions: The prevalence of self-reported asthma among Swedish competitive recreational endurance athletes appears to be higher than that in the general Swedish population. A large proportion of recreational athletes were reported with asthma use medications, indicating an association between high physical activity and self-reported asthma among competitive recreational athletes.

  • 215. O'Byrne, Paul M
    et al.
    Inman, Mark D
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Reassessing the Th2 cytokine basis of asthma.2004In: Trends Pharmacol Sci, ISSN 0165-6147, Vol. 25, no 5, p. 244-8Article in journal (Refereed)
  • 216. O'Byrne, Paul M
    et al.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Beta2 deja vu.2006In: Chest, ISSN 0012-3692, Vol. 129, no 1, p. 3-5Article in journal (Refereed)
  • 217. Olin, A C
    et al.
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Torén, K
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Helleday, Ragnberth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Ledin, M C
    Ljungkvist, G
    Ekman, A
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Nitric oxide (NO) in exhaled air after experimental ozone exposure in humans2001In: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 95, no 6, p. 491-495Article in journal (Refereed)
    Abstract [en]

    We hypothesized that ozone, a common air pollutant, potent in producing airway inflammation, would increase the production of exhaled nitric oxide (NO). If so, measurement of exhaled NO could potentially be a valuable tool in population studies of air pollution effects. Eleven healthy non-smoking volunteers were exposed to 0.2 ppm ozone (O3) and filtered air for 2h on two separate occasions. Exhaled NO and nasal NO were measured before and on five occasions following the exposures. Changes in exhaled and nasal NO after ozone exposure were adjusted for changes after air exposure. There was a slight decrease in exhaled NO (-0.6; -3.1-1.2 ppb) (median and 95% confidence interval) and of nasal NO (-57; -173-75 ppb) directly after the ozone exposure. No significant changes in exhaled or nasal NO were however found 6 or 24 h after the exposure. Within the examined group, an O3 exposure level proven to induce an airway inflammation caused no significant changes in exhaled or nasal NO levels. Hence, the current study did not yield support for exhaled NO as a useful marker of ozone-induced oxidative stress and airway inflammation after a single exposure. This contrasts with data for workers exposed to repeated high peaks of ozone. The potential for exhaled NO as a marker of oxidative stress therefore deserves to be further elucidated.

  • 218. Omenaas, E
    et al.
    Svanes, C
    Janson, C
    Toren, K
    Jogi, R
    Gislason, T
    Franklin, Karl
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Gulsvik, A
    What can we learn about asthma and allergy from the follow-up of the RHINE and the ECRHS studies?2008In: The Clinical Respiratory Journal, Vol. 2, no 1, p. 45-52Article in journal (Refereed)
  • 219.
    Persson, Hampus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Asthma control and asthma medication usage among elite endurance athletes2016Independent thesis Basic level (professional degree), 20 credits / 30 HE creditsStudent thesis
  • 220.
    Pourazar, Jamshid
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Helleday, Ragnberth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Muala, Ala
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Rankin, Gregory
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sehlstedt, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Unosson, Jon
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Langrish, J. P.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bosson, Jenny A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Airway Inflammatory Response In Healthy Subjects Following Chamber Exposure To 100% Rme Biodiesel2015In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 191, article id A5252Article in journal (Other academic)
  • 221.
    Pourazar, Jamshid
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Kelly, Frank J
    Davies, Donna E
    Wilson, Susan J
    Holgate, Stephen T
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Diesel exhaust increases EGFR and phosphorylated C-terminal Tyr 1173 in the bronchial epithelium2008In: Particle and Fibre Toxicology, ISSN 1743-8977, E-ISSN 1743-8977, Vol. 5, article id 8Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Epidemiological studies have demonstrated adverse health effects of environmental pollution. Diesel exhaust (DE) is a major contributor to particulate matter pollution. DE exposure has been shown to induce a pronounced inflammatory response in the airways, together with an enhanced epithelial expression of cytokines such as IL-8, Gro-alpha, IL-13 and activation of redox sensitive transcription factors (NFkappaB, AP-1), and MAP kinases (p38, JNK). The aim of the present investigation was to elucidate the involvement of the epidermal growth factor receptor (EGFR) signalling pathway in the epithelial response to DE in-vivo.

    RESULTS: Immunohistochemical staining was used to quantify the expression of the EGFR, phosphorylated Tyrosine residues, MEK and ERK in the bronchial epithelium of archived biopsies from 15 healthy subjects following exposure to DE (PM10, 300 mug/m3) and air. DE induced a significant increases in the expression of EGFR (p = 0.004) and phosphorylated C-terminal Tyr 1173 (p = 0.02). Other investigated EGFR tyrosine residues, Src related tyrosine (Tyr 416), MEK and ERK pathway were not changed significantly by DE.

    CONCLUSION: Exposure to DE (PM10, 300 mug/m3) caused enhanced EGFR expression and phosphorylation of the tyrosine residue (Tyr 1173) which is in accordance with the previously demonstrated activation of the JNK, AP-1, p38 MAPK and NFkB pathways and associated downstream signalling and cytokine production. No effects were seen on the MEK and ERK pathway suggesting that at the investigated time point (6 hours post exposure) there was no proliferative/differentiation signalling in the bronchial epithelium. The present findings suggest a key role for EGFR in the bronchial response to diesel exhaust.

  • 222.
    Pourazar, Jamshid
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Frew, Anthony J
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Helleday, Ragnberth
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Kelly, Frank J
    Wilson, Susan
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Diesel exhaust exposure enhances the expression of IL-13 in the bronchial epithelium of healthy subjects.2004In: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 98, no 9, p. 821-825Article in journal (Refereed)
    Abstract [en]

    Epidemiological studies have demonstrated adverse health effects of environmental pollution. Diesel exhaust (DE) is an important contributor to ambient particulate matter pollution. DE exposure has been shown to induce a pronounced inflammatory response in the airways, with an enhanced epithelial expression of IL-8, and Gro-α in healthy subjects. The present investigation was aimed to further characterise the epithelial response to DE in vivo, with particular reference to possible TH2 response, in non-atopic healthy subjects. To determine this response, 15 healthy, non-atopic non-smoking subjects with normal lung function were exposed to DE (PM10 300 μg/m3) and filtered air during 1 h on two separate randomised occasions. Bronchoscopy sampling of bronchial mucosal biopsies was performed 6 h after exposure. Immunohistochemical staining were performed using mAb for IL-10, IL-13 and IL-18 expression. DE exposure induced a significant increase in the expression of IL-13 in the bronchial epithelium cells, 2.1 (1.35–4.88) Md (Q1–Q3) vs. air 0.94 (0.53–1.23); P=0.009. No significant changes were seen in IL-10 and IL-18 expression. This finding suggests an TH2-inflammatory response in the airways of non-atopic healthy individuals.

  • 223. Pérez-Chada, Daniel
    et al.
    Videla, Alejandro J
    O'Flaherty, Martin E
    Majul, Claudio
    Catalini, Ana M
    Caballer, Carlos A
    Franklin, Karl
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Snoring, witnessed sleep apnoeas and pregnancy-induced hypertension.2007In: Acta Obstet Gynecol Scand, ISSN 0001-6349, Vol. 86, no 7, p. 788-92Article in journal (Refereed)
  • 224.
    Qvist, Linnea
    et al.
    Stockholm, Sweden.
    Nilsson, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johansson, Viktor
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Larsson, Kjell
    Stockholm, Sweden.
    Rönmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Langrish, Jeremy
    Edinburgh, United Kingdom.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lindberg, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Central arterial stiffness is increased among subjects with severe and very severe COPD: report from a population-based cohort study2015In: European Clinical Respiratory Journal, ISSN 2001-8525, Vol. 2, article id 27023Article in journal (Refereed)
    Abstract [en]

    Introduction: Cardiovascular disease (CVD) is common in chronic obstructive pulmonary disease (COPD) and is, as productive cough, related to poorer prognosis in COPD. Central arterial stiffness is a marker of early atherosclerosis, but the association between COPD, productive cough, and arterial stiffness as a possible indicator of CVD is unclear.

    Objectives: To compare both arterial stiffness among subjects with and without COPD and the impact of productive cough in a population-based cohort.

    Methods: A population-based cohort, including 993 COPD and 993 non-COPD subjects, has been invited to annual examination since 2005. In 2010, 947 subjects, of which 416 had COPD (according to the GOLD spirometric criteria), participated in examinations including structured interview, spirometry, and measurements of central arterial stiffness as pulse wave velocity (PWV).

    Results: PWV was higher in GOLD 3–4 compared to non-COPD (10.52 vs. 9.13 m/s, p=0.042). CVD and age ≥60 were both associated with significantly higher PWV in COPD as well as in non-COPD. In COPD, those with productive cough had higher PWV than those without, significantly so in GOLD 1 (9.59 vs. 8.92 m/s, p=0.024). In a multivariate model, GOLD 3–4 but not productive cough was associated with higher PWV, when adjusted for sex, age group, smoking habits, blood pressure, CVD, and pulse rate.

    Conclusions: GOLD 3–4, age ≥60, and CVD were associated with increased arterial stiffness, and also increased in COPD subjects with productive cough compared to those without. Of importance, GOLD 3–4 but not productive cough remained associated with increased central arterial stiffness when adjusted for confounders.

  • 225.
    Rademaekers, Max
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Longitudinal Acute Air Pollution Systemic Effects (LAPSE)A study of the systemic effects of diesel exhaust exposure2015Independent thesis Basic level (professional degree), 20 credits / 30 HE creditsStudent thesis
  • 226.
    Ramstedt, Madeleine
    et al.
    Umeå University, Faculty of Science and Technology, Chemistry.
    Ekstrand-Hammarström, Barbro
    Shchukarev, Andrey
    Umeå University, Faculty of Science and Technology, Chemistry.
    Bucht, Anders
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Österlund, Lars
    Welch, Martin
    Huck, Wilhelm T.S.
    Bacterial and mammalian cell response to poly(3-sulfopropyl methacrylate) brushes loaded with silver halide salts2009In: Biomaterials, Vol. 30, no 8, p. 1524-31Article in journal (Refereed)
    Abstract [en]

    This study investigates the antibacterial and cytotoxic effect of surfaces with sulphonate brushes containing silver salts. By using the same type of samples for both cytotoxicity and antibacterial studies, these two parameters could be compared in a controlled way. The silver was incorporated into the brush in four different forms to enable release of silver ions at different concentrations and different rates. It was found that although the surfaces displayed very good antibacterial properties in buffer solutions, this effect disappeared in systems with high protein content. Similarly, the silver-containing surfaces displayed cytotoxic effects in the absence of serum proteins but this effect was reduced in the presence of serum. The speciation of silver in the different solutions is discussed. Cytotoxic and antibacterial effects are compared at the different silver concentrations released. The implications of a concentration range where silver could be used to kill bacterial without harmful effects on mammalian cells are also discussed and questioned.

  • 227.
    Rankin, Gregory D.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Rasmuson, Johan
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ahlm, Clas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Immunolocalisation Of Puumala Hantavirus In Human Endobronchial Biopsies2015In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 191, article id A3793Article in journal (Other academic)
  • 228.
    Rankin, Gregory D.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Thomas, S.
    Baharom, F.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ahlm, Clas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Smed-Sorensen, A.
    Distribution Of Human Respiratory Dendritic Cell Subsets At Steady State Differs In Specific Compartments Of The Airways2015In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 191, article id A1300Article in journal (Other academic)
  • 229.
    Rankin, Gregory D.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Wingfors, Håkan
    Swedish Defence Research Agency, CBRN Defence and Security, Umeå, Sweden..
    Uski, Oskari
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Hedman, Linnéa
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Department of Health Sciences, Division of Nursing, Luleå University of Technology, Luleå, Sweden..
    Ekstrand-Hammarström, Barbro
    Swedish Defence Research Agency, CBRN Defence and Security, Umeå, Sweden..
    Bosson, Jenny
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundbäck, Magnus
    Karolinska Institutet, Department of Clinical Sciences, Division of Cardiology, Danderyd University Hospital, Stockholm, Sweden..
    The toxic potential of a fourth-generation E-cigarette on human lung cell lines and tissue explants2019In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 39, no 8, p. 1143-1154Article in journal (Refereed)
    Abstract [en]

    The use of electronic cigarettes (E‐cigs) is rapidly increasing. The latest generation of E‐cigs is highly customizable, allowing for high heating coil temperatures. The aim of this study was to assess the toxic potential of a fourth‐generation E‐cig. Aerosols generated from E‐liquid with (24 mg/mL) and without nicotine, using a fourth‐generation E‐cig, were chemically analysed and compared with cigarette smoke (K3R4F). Human lung epithelial cell lines and distal lung tissue explants were exposed to E‐cig vapour extract (EVE) and cigarette smoke extract for 24 hours and assessed for viability, inflammation, oxidative stress and genotoxicity. E‐cig aerosols contained measurable levels of volatile organic compounds, aldehydes and polycyclic aromatic hydrocarbons, in general, to a much lesser extent than cigarette smoke. Higher levels of certain carbonyls, e.g. formaldehyde, were detected in the E‐cig aerosols. EVEs decreased cell viability of BEAS‐2B cells, whereas little effect was seen in A549 cells and distal lung tissue. The nicotine‐containing EVE caused a greater decrease in cell viability and significant increase in DNA damage than the nicotine‐free EVE. Increased cytotoxicity, reactive oxygen species production and genotoxicity were seen with cells and tissue exposed to cigarette smoke extract compared with EVEs. Although E‐cig aerosols were less toxic than cigarette smoke, it was not benign. Moreover, the EVE containing nicotine was more toxic than the nicotine‐free EVE. More research is needed on the short‐ and long‐term health effects of vaping and the usage of newly emerging E‐cig devices to evaluate better the potential negative effects of E‐cigs on human health.

  • 230.
    Rasmuson, Johan
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Andersson, Charlotta
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Norrman, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Haney, Michael
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Evander, Magnus
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Ahlm, Clas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Time to revise the paradigm of hantavirus syndromes? Hantavirus pulmonary syndrome caused by European hantavirus2011In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 30, no 5, p. 685-690Article in journal (Refereed)
    Abstract [en]

    Hantaviruses have previously been recognised to cause two separate syndromes: hemorrhagic fever with renal syndrome in Eurasia, and hantavirus pulmonary syndrome (HPS) in the Americas. However, increasing evidence suggests that this dichotomy is no longer fruitful when recognising human hantavirus disease and understanding the pathogenesis. Herein are presented three cases of severe European Puumala hantavirus infection that meet the HPS case definition. The clinical and pathological findings were similar to those found in American hantavirus patients. Consequently, hantavirus infection should be considered as a cause of acute respiratory distress in all endemic areas worldwide.

  • 231.
    Rasmuson, Johan
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Sörensen, Karen
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Hedström, Magnus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ahlm, Clas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Cardiopulmonary involvement in Puumala hantavirus infection2013In: BMC Infectious Diseases, ISSN 1471-2334, E-ISSN 1471-2334, Vol. 13, no 1, p. 501-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Hantavirus infections cause potentially life-threatening disease in humans world-wide. Infections with American hantaviruses may lead to hantavirus pulmonary syndrome characterised by severe cardiopulmonary distress with high mortality. Pulmonary involvement in European Puumala hantavirus (PUUV) infection has been reported, whereas knowledge of potential cardiac manifestations is limited. We aimed to comprehensively investigate cardiopulmonary involvement in patients with PUUV-infection.

    METHODS: Twenty-seven hospitalised patients with PUUV-infection were examined with lung function tests, chest high-resolution CT (HRCT), echocardiography including speckle tracking strain rate analysis, ECG and measurements of cardiac biomarkers N-terminal pro-B-type natriuretic peptide (NT-ProBNP) and troponin T. Patients were re-evaluated after 3 months. Twenty-five age and sex-matched volunteers acted as controls for echocardiography data.

    RESULTS: Two-thirds of the patients experienced respiratory symptoms as dry cough or dyspnoea. Gas diffusing capacity was impaired in most patients, significantly improving at follow-up but still subnormal in 38%. HRCT showed thoracic effusions or pulmonary oedema in 46% of the patients. Compared to controls, the main echocardiographic findings in patients during the acute phase were significantly higher pulmonary vascular resistance, higher systolic pulmonary artery pressure, lower left ventricular ejection fraction and impaired left atrial myocardial motion. Pathological ECG, atrial fibrillation or T-wave changes, was demonstrated in 26% of patients. NT-ProBNP concentrations were markedly increased and were inversely associated with gas diffusing capacity but positively correlated to pulmonary vascular resistance. Furthermore, patients experiencing impaired general condition at follow-up had significantly lower gas diffusing capacity and higher pulmonary vascular resistance, compared to those feeling fully recovered.

    CONCLUSIONS: In a majority of patients with PUUV-infection, both cardiac and pulmonary involvement was demonstrated with implications on patients' recovery. The results demonstrate vascular leakage in the lungs that most likely is responsible for impaired gas diffusing capacity and increased pulmonary vascular resistance with secondary pulmonary hypertension and right heart distress. Interestingly, NT-ProBNP was markedly elevated even in the absence of overt ventricular heart failure. The method of simultaneous investigations of important cardiac and respiratory measurements improves the interpretation of the underlying pathophysiologic mechanisms.

  • 232.
    Rasmuson, Johan
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Linderholm, Mats
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ahlm, Clas
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
    Presence of activated airway T lymphocytes in human puumala hantavirus disease2011In: Chest, ISSN 0012-3692, E-ISSN 1931-3543, Vol. 140, no 3, p. 715-722Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Hantaviruses cause two clinical syndromes; hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The clinical spectrum in HFRS also often involves respiratory symptoms. As information of the pulmonary pathogenesis in HFRS is limited, we aimed to further study the local airway immune response in the lower airways.

    METHODS: In 15 hospitalized HFRS patients, bronchoscopy was performed with sampling of endobronchial mucosal biopsies and bronchoalveolar lavage (BAL) fluid. Biopsies were stained for leukocytes, lymphocyte subsets and vascular endothelial adhesion molecules. BAL fluid and blood lymphocyte subsets were determined using flow cytometry. Fourteen healthy volunteers acted as control group.

    RESULTS: Compared to controls, endobronchial mucosal biopsies from HFRS patients revealed increased numbers of CD8(+) T cells in both epithelium and submucosa (p≤0.001), along with an increase in submucosal CD4(+) T cells (p=0.001). In contrast, patients' submucosal neutrophil and eosinophil numbers were reduced (p<0.001). The expression of vascular cell adhesion molecule-1 (VCAM-1) was enhanced in HFRS patients (p<0.001). In HFRS patients, analyses of T cell subsets in BAL fluid showed higher proportions of CD3(+) and CD8(+) T cells (p=0.011 and p=0.025), NK cells (p<0.001) together with an increased expression of activation markers HLA-DR and CD25 on T cells (p<0.001 and p<0.001).

    CONCLUSIONS: The present findings indicate a local immune response in terms of activated T lymphocytes in the lungs of patients with HFRS. The elevated expression of activation markers and VCAM-1 further implies the importance of cytotoxic lymphocytes in the pathogenesis of pulmonary involvement in HFRS.

  • 233. Riihimäki, Miia
    et al.
    Raine, Amanda
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Art, Tatiana
    Lekeux, Pierre
    Couëtil, Laurent
    Pringle, John
    Epithelial expression of mRNA and protein for IL-6, IL-10 and TNF-alpha in endobronchial biopsies in horses with recurrent airway obstruction.2008In: BMC veterinary research, ISSN 1746-6148, Vol. 4, p. 8-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The aim of this study was to evaluate the contribution of bronchial epithelium to airway inflammation, with focus on mRNA and protein expression of cytokines of innate immunity IL-6, IL-10 and TNF-alpha, in horses with Recurrent Airway Obstruction (RAO) during exacerbation and in remission. RESULTS: Despite marked clinical and physiologic alterations between exacerbation and after remission in the RAO horses no differences were detected in either cytokine mRNA or protein levels. Moreover, the expression of investigated cytokines in RAO horses on pasture did not differ from controls.In comparing real-time PCR analysis to results of immunohistochemistry only IL-10 mRNA and protein levels in RAO horses on pasture were significantly correlated (rs = 0.893, p = 0.007). Curiously, in controls examined on pasture the TNF-alpha protein level was positively correlated to IL-10 mRNA expression (rs = 0.967, p = 0.007) and negatively correlated to IL-6 mRNA expression (rs = -0.971, p = 0.001). CONCLUSION: Given the complementary relationship of assessing cytokines directly by immunohistochemistry, or indirectly by PCR to mRNA, the lack of significant changes in either mRNA or protein levels of IL-6, IL-10 or TNF-alpha mRNA in RAO horses in exacerbation suggests that these particular cytokines in bronchial tissue may not play a substantive role in the active inflammation of this disease. To support this contention further studies examining time dependency of expression of IL-6, IL-10 or TNF-alpha are needed, as is expansion of the range of cytokines to include other key regulators of airway inflammation.

  • 234. Rissle, Jenny
    et al.
    Swietlicki, Erik
    Bengtsson, Agneta
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics, Energy Technology and Thermal Process Chemistry.
    Pagels, Joakim
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Londahl, Jakob
    Corrigendum to "Experimental determination of deposition of diesel exhaust particles in the human respiratory tract": [J. Aerosol Sci. vol 48(2012) 18-33]2012In: Journal of Aerosol Science, ISSN 0021-8502, E-ISSN 1879-1964, Vol. 51, p. 81-81Article in journal (Refereed)
  • 235. Rissler, Jenny
    et al.
    Swietlicki, Erik
    Bengtsson, Agneta
    Boman, Christoffer
    Pagels, Joakim
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Löndahl, Jakob
    Experimental determination of deposition of diesel exhaust particles in the human respiratory tract2012In: Journal of Aerosol Science, ISSN 0021-8502, E-ISSN 1879-1964, Vol. 48, p. 18-33Article in journal (Refereed)
    Abstract [en]

    Diesel emissions are a major contributor to combustion-generated airborne ambient particles. To understand the role of diesel particulate emissions on health effects, it is important to predict the actual particulate dose deposited in the human respiratory tract, with respect to number, surface area and mass. This is complicated by the agglomerate nature of some of these particles. In this study the respiratory tract deposition fraction in the size range 10-500 nm, was determined for 10 healthy volunteers during both idling and transient engine running conditions of a heavy duty diesel engine. The aerosol was characterized with respect to both chemical and physical properties including size resolved particle effective density. The dominating part of the emitted particles had an agglomerate structure. For those formed during transient running conditions, the relationship between particle mass and mobility diameter could be described by a power law function. This was not the case during idling, most likely because of volatile compounds condensing on the agglomerates. The respiratory tract particle deposition revealed large intra-subject variability with some subjects receiving a dose that was twice as high as that of others, when exposed to the same particle concentration. Associations were found between total deposited fractions (TDF), and breathing pattern. There was a difference between the idling and transient cycle with TDF being higher with respect to number during idling. The measured size-dependent deposition fraction of the agglomerated exhaust particles from both running conditions was nearly identical and closely resembled that of spherical hydrophobic particles, if plotted as a function of mobility diameter. Thus, for the size range covered, the mobility diameter could well describe the diameter-dependent particle respiratory tract deposition probability, regardless of the agglomeration state of the particles. Whilst mobility diameter well describes the deposition fraction, more information about particle characteristics is needed to convert this to volume equivalent diameter or estimate dose with respect to surface area or mass. A methodology is presented and applied to calculate deposited dose by surface area and mass of agglomerated particles. The methodology may be useful in similar studies estimating dose to the lung, deposition onto cell cultures and in animal studies. (C) 2012 Elsevier Ltd. All rights reserved.

  • 236. Robb, A O
    et al.
    Din, J N
    Mills, N L
    Smith, I B J
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Zikry, M N L
    Raftis, J B
    Newby, D E
    Denison, F C
    The influence of the menstrual cycle, normal pregnancy and pre-eclampsia on platelet activation2010In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 103, no 2, p. 372-378Article in journal (Refereed)
    Abstract [en]

    Platelet activation has a key role in mediating thrombotic and inflammatory events. This study aimed to determine the influence of the menstrual cycle, pregnancy and pre-eclampsia on in vivo platelet activation. Twelve healthy nulliparous, non-smoking women with regular menses were studied over a single menstrual cycle. Twenty-one healthy primigravida pregnant women were studied longitudinally at 16, 24, 32 and 37 weeks gestation and seven weeks post-partum. Sixteen primigravida women with pre-eclampsia were studied at time of diagnosis and at seven weeks post-partum. Platelet-monocyte aggregates and platelet-surface P-selectin expression were assessed by flow-cytometry. Soluble P-selectin and CD40 ligand (CD40L) were measured by ELISA. Markers of platelet activation did not vary over the menstrual cycle. Platelet-monocyte aggregates were greater in the third trimester of pregnancy compared to non-pregnant women (p=0.003). Platelet surface and plasma soluble P-selectin concentrations increased with gestation (p<0.0001) and were raised by 24 weeks of pregnancy compared to non-pregnant women (p< or =0.02 for both) and together with platelet monocyte aggregates, decreased post-partum (p< or =0.02). Soluble CD40L concentrations fell in pregnancy, reaching a nadir at mid-gestation (p=0.002). There were no differences in markers of platelet activation between normal and pre-eclamptic pregnancies. In conclusion, platelet activation is increased in pregnancy and increases with gestation but is unaffected by pre-eclampsia. This suggests that systemic platelet activation is a feature of pregnancy but this is not affected by established pre-eclampsia.

  • 237. Robb, A O
    et al.
    Mills, N L
    Smith, I B J
    Short, A
    Tura-Ceide, O
    Barclay, G R
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Critchley, H O D
    Newby, D E
    Denison, F C
    Influence of menstrual cycle on circulating endothelial progenitor cells2009In: Human Reproduction, ISSN 0268-1161, E-ISSN 1460-2350, Vol. 24, no 3, p. 619-625Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Endothelial progenitor cells (EPCs) are circulating mononuclear cells that participate in angiogenesis. The aim of this study was to determine the influence of the menstrual cycle on the number and function of EPCs, and to investigate their relationship with circulating concentrations of sex steroids and inflammatory mediators. METHODS: Ten healthy nulliparous, premenopausal, non-smoking women with regular menses were studied over a single menstrual cycle. Venepuncture was performed in the menstrual, follicular, peri-ovulatory and luteal phases. EPCs were quantified by flow cytometry (CD133(+)CD34(+)KDR(+) phenotype) and the colony-forming unit (CFU-EPC) functional assay. Circulating concentrations of estradiol, progesterone and inflammatory mediators (TNF-alpha, IL-6, sICAM-1 and VEGF) were measured by immunoassays. RESULTS: The numbers of CD133(+)CD34(+)KDR(+) cells were higher in the follicular phase (0.99 +/- 0.3 x 10(6) cells/l) compared with the peri-ovulatory phase (0.29 +/- 0.1 x 10(6) cells/l; P < 0.05). In contrast, the numbers of CFU-EPCs did not vary over the menstrual cycle. There were no correlations between EPCs and concentrations of either circulating sex steroids or inflammatory mediators. CONCLUSIONS: CD133(+)CD34(+)KDR(+) cells but not CFU-EPCs vary during the menstrual cycle. Our findings suggest a potential role for circulating EPCs in the normal cycle of physiological angiogenesis and repair of the uterine endometrium that is independent of circulating sex steroids or inflammatory mediators.

  • 238.
    Rocksén, David
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine.
    Koch, Bo
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Bucht, Anders
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine.
    Lung effects during a generalized Shwartzman reaction and therapeutic intervention with dexamethasone or vitamin E.2004In: Shock, ISSN 1073-2322, Vol. 22, no 5, p. 482-90Article in journal (Refereed)
  • 239. Rogers, Andrew V
    et al.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Hattotuwa, Keith
    Dewar, Ann
    Jeffery, Peter K
    Bronchial mucosal dendritic cells in smokers and ex-smokers with COPD: an electron microscopic study.2007In: Thorax, ISSN 0040-6376Article in journal (Refereed)
  • 240.
    Roos-Engstrand, Ester
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    T cells in chronic obstructive pulmonary disease2010Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Background: Tobacco smoking is the main cause of chronic obstructive pulmonary disease, COPD, but the mechanisms by which cigarette smoke induces COPD are still elusive. T lymphocytes have been implicated in the pathogenesis of the disease, but their role in the airway inflammation in COPD is not fully understood. The aim of this thesis was therefore to address T lymphocyte subsets and their activation in the airways of subjects with COPD, in comparison to smokers with normal lung function (S) and never smokers (NS).

    Methods: Subjects with moderate to severe COPD were recruited along with controls. They were all non-atopic and clinically stable, without any exacerbation during at least three months prior to inclusion. Only medication with short-acting β2-agonists and/or anti-cholinergic drugs was permitted. All subjects underwent bronchoscopy with endobronchial mucosal biopsy sampling as well as bronchial wash, BW, and bronchoalveolar lavage, BAL, collection. Biopsies were immunohistochemically stained for inflammatory cells and markers. BW and BAL fluids were prepared for differential cell counts. Soluble markers were measured in BW and lymphocyte subsets were determined in BAL using flow cytometry.

    Results: In biopsies, an increase in epithelial CD3+ and CD8+ cells was found in COPD, compared to NS. In BAL fluid, CD8+ cells were enhanced, whereas CD4+ cells were reduced in subjects with COPD and S, compared to NS. Furthermore, CD4+ and CD8+ cells were more activated both in COPD and S, in terms of increased expression of CD25, CD69 and HLA-DR. NKG2D-expressing CD8+ T cells in BAL fluid were enhanced in both COPD and S. CD4+CD25bright cells were upregulated in COPD and S, suggesting the presence of regulatory T cells. Further analyses of T cell subsets with the more specific markers for regulatory T cells, FoxP3 and CD127, indicated a smoking-induced expansion of non-regulatory T cells, which tended to normalize after smoking cessation in COPD. Currently smoking subjects with COPD still expressed high proportions of activated non-regulatory CD4+ T cells. The data on FoxP3 expression further indicated that the increase in CD25 expression in COPD and S was not only associated with the expansion of regulatory T cells. As CD127 expression is reported to be inversely associated with FoxP3, the data indicate the expansion of a non-regulatory CD25+ population in smokers and patients with stable COPD. The immunohistochemical staining for the NKG2D ligands MICA and MICB on epithelial cells was unchanged.

    Conclusion: The results of this thesis suggest a role for CD4+ and CD8+ T-cells in clinically stable COPD, indicating that T-cells are of importance in the long-term inflammatory response in COPD. Regardless of current smoking habits, activated CD8+ T lymphocytes were found to be increased in BAL fluid from subjects with COPD, suggesting that changes in CD8+ T cells are associated with a persistent immune response and, thus, of importance in COPD pathogenesis. In contrast, the expansion of non-regulatory CD25+CD4+ cells in BAL fluid seemed to be preferentially smoke-related. In summary, the data indicate that, among airway T cells, changes in CD8+ cells seem to be highly associated with COPD pathogenesis, whereas changes in CD4+ cells appear to be related to cigarette smoke-induced responses. Further, a non regulatory population of helper T cells was identified in BAL fluid of COPD patients, which may contribute to the persistent cytotoxic T cell responses.

  • 241.
    Roos-Engstrand, Ester
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ekstrand-Hammarström, Barbro
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bucht, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Influence of smoking cessation on airway T lymphocyte subsets in COPD2009In: COPD, ISSN 1541-2563, Vol. 6, no 2, p. 112-120Article in journal (Refereed)
    Abstract [en]

    The mechanisms behind airway inflammation in chronic obstructive pulmonary disease (COPD) are still not well understood. Here we investigated lymphocyte subtypes in bronchoalveolar lavage fluid, likely to be involved in the pathogenesis of COPD, as well as exploring the effect of smoking cessation. Differential cell counts and T cell subsets were determined in BAL fluid from nineteen individuals with stable COPD (seven smokers, twelve ex-smokers) compared to twelve age-matched never-smokers and thirteen smoking-matched smokers with normal lung function. COPD-patients had higher percentages of airway CD8(+) T cells compared to never-smokers. An increased population of CD4(+) T cells expressed high levels of CD25 in smokers and COPD patients compared to never-smokers, suggesting the presence of regulatory T cells. As the T cell populations in smokers with normal lung function and COPD-patients were similar, the impact of current smoking in COPD was addressed in a subgroup analysis. Activation of CD8(+) T cells was found regardless of smoking habits. In contrast, the enhanced expression of gamma/delta T cells, was mainly associated with current smoking, whilst the increase in T regulatory cells appeared related to both smoking and COPD. Regardless of smoking habits, CD8(+) T cell activation was found in COPD, supporting the contention that this T cell subset may play a role in the pathogenesis of COPD. As CD8(+) T cells coexist with immunoregulatory CD4(+) T cells in airways of COPD patients, it is likely that both cytotoxic T-cell responses and immunosuppressive mechanisms may be of importance in COPD pathogenesis.

  • 242.
    Roos-Engstrand, Ester
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bucht, Anders
    Swedish Defence Research Agency, Division of CBRN Defence and Security, Umeå, Sweden.
    Cytotoxic T cells expressing the co-stimulatory receptor NKG2D are increased in cigarette smoking and COPD2010In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 11, p. 128-Article in journal (Refereed)
    Abstract [en]

    Background: A suggested role for T cells in COPD pathogenesis is based on associations between increased lung cytotoxic T lymphocyte (CD8+) numbers and airflow limitation. CD69 is an early T cell activation marker. NKG2D receptors are co-stimulatory molecules induced on CD8+ T cells upon activation. The activating function of NKG2D is triggered by binding to the MHC class 1 chain-related (MIC) molecules A and B, expressed on surface of stressed epithelial cells. The aim of this study was to evaluate the expression of MIC A and B in the bronchial epithelium and NKG2D and CD69 on BAL lymphocytes in subjects with COPD, compared to smokers with normal lung function and healthy never-smokers.

    Methods: Bronchoscopy with airway lavages and endobronchial mucosal biopsy sampling was performed in 35 patients with COPD, 21 healthy never-smokers and 16 smokers with normal lung function. Biopsies were immunohistochemically stained and BAL lymphocyte subsets were determined using flow cytometry.

    Results: Epithelial CD3+ lymphocytes were increased in both smokers with normal lung function and in COPD patients, compared to never-smokers. Epithelial CD8+ lymphocyte numbers were higher in the COPD group compared to never-smoking controls. Among gated CD3+cells, the percentage of CD8+ NKG2D+ cells was enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. The percentage of CD8+ CD69+ cells and cell surface expression of CD69 were enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. No changes in the expression of MIC A or MIC B in the airway epithelium could be detected between the groups, whereas significantly decreased soluble MICB was detected in bronchial wash from smokers with normal lung function, compared to never-smokers.

    Conclusions: In COPD, we found increased numbers of cytotoxic T cells in both bronchial epithelium and airway lumen. Further, the proportions of CD69- and NKG2D-expressing cytotoxic T cells in BAL fluid were enhanced in both subjects with COPD and smokers with normal lung function and increased expression of CD69 was found on CD8+ cells, indicating the cigarette smoke exposure-induced expansion of activated cytotoxic T cells, which potentially can respond to stressed epithelial cells.

  • 243.
    Roos-Engstrand, Ester
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bucht, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Expansion of CD4+CD25+ helper T cells without regulatory function in smoking and COPD2011In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 12, no 74, p. 8-Article in journal (Refereed)
    Abstract [en]

    Background: Regulatory T cells have been implicated in the pathogenesis of COPD by the increased expression of CD25 on helper T cells along with enhanced intracellular expression of FoxP3 and low/absent CD127 expression on the cell surface.

    Method: Regulatory T cells were investigated in BALF from nine COPD subjects and compared to fourteen smokers with normal lung function and nine never-smokers.

    Results: In smokers with normal lung function, the expression of CD25+CD4was increased, whereas the proportions of FoxP3and CD127were unchanged compared to never-smokers. Among CD4+cells expressing high levels of CD25, the proportion of FoxP3cells was decreased and the percentage of CD127was increased in smokers with normal lung function. CD4+CD25cells with low/absent CD127 expression were increased in smokers with normal lung function, but not in COPD, when compared to never smokers.

    Conclusion: The reduction of FoxP3 expression in BALF from smokers with normal lung function indicates that the increase in CD25 expression is not associated with the expansion of regulatory T cells. Instead, the high CD127 and low FoxP3 expressions implicate a predominantly non-regulatory CD25helper T-cell population in smokers and stable COPD. Therefore, we suggest a smoking-induced expansion of predominantly activated airway helper T cells that seem to persist after COPD development.

  • 244.
    Roos-Engstrand, Ester
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bucht, Anders
    Swedish Defence Research Agency, Division of CBRN Defence and Security, Umeå, Sweden.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Expansion of helper T cells with a non-regulatory function in smoking and COPDManuscript (preprint) (Other academic)
    Abstract [en]

    Regulatory T cells have been implicated in the pathogenesis of COPD by the increased expression of CD25 on helper T cells. Regulatory CD4+ T cells are reported to have increased intracellular expression of FoxP3 and low/absent CD127 expression on the cell surface. Here, these markers were investigated in BALF from nine COPD subjects and compared to fourteen smokers with normal lung function and nine never-smokers.

    In smokers with normal lung function, the expression of CD25 on CD4+ lymphocytes was increased, whereas the proportions of FoxP3+ and CD127+ were unchanged compared to never-smokers. Among the population of helper T cells expressing high levels of CD25, the proportion FoxP3+ cells was decreased and the percentage CD127+ was increased in smokers with normal lung function. CD25+ helper T cells with low/absent CD127 expression were increased in smokers with normal lung function, but not in COPD, when compared to never smokers. In COPD, a decrease in CD127 expression on CD4+CD25+ was observed in ex-smokers compared to current smokers.

    Smoking induces the expansion of activated airway helper T cells that seem to persist after COPD development. The reduction of FoxP3 expression indicates that the increase in CD25 expression is not only associated with the expansion of regulatory T cells. Instead, the high CD127 and low FoxP3 expressions implicate a predominantly non-regulatory CD25+ helper T cell population in stable COPD. In some smokers with normal lung function, we identified a helper T cell population with a putative regulatory function, which may be protective against COPD development.

  • 245.
    Rzhepishevska, Olena
    et al.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Hakobyan, Shoghik
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Ekstrand-Hammarström, Barbro
    Swedish Defense Research Institute (FOI), Umeå, Sweden.
    Nygren, Yvonne
    Swedish Defense Research Institute (FOI), Umeå, Sweden.
    Karlsson, Torbjörn
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Bucht, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Swedish Defense Research Institute (FOI), Umeå, Sweden.
    Elofsson, Mikael
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Boily, Jean-François
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Ramstedt, Madeleine
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    The gallium(III)-salicylidene acylhydrazide complex shows synergistic anti-biofilm effect and inhibits toxin production by Pseudomonas aeruginosa2014In: Journal of Inorganic Biochemistry, ISSN 0162-0134, E-ISSN 1873-3344, Vol. 138, p. 1-8Article in journal (Refereed)
    Abstract [en]

    Bacterial biofilms cause a range of problems in many areas and especially in health care. Biofilms are difficult to eradicate with traditional antibiotics and consequently there is a need for alternative ways to prevent and/or remove bacterial biofilms. Furthermore, the emergence of antibiotic resistance in bacteria creates a challenge to find new types of antibiotics with a lower evolutionary pressure for resistance development. One route to develop such drugs is to target the so called virulence factors, i.e. bacterial systems used when bacteria infect a host cell. This study investigates synergy effects between Ga(III) ions, previously reported to suppress biofilm formation and growth in bacteria, and salicylidene acylhydrazides (hydrazones) that have been proposed as antivirulence drugs targeting the type three secretion system used by several Gram-negative pathogens, including Pseudomonas aerugionosa, during bacterial infection of host cells. A library of hydrazones was screened for: Fe(III) binding, enhanced anti-biofilm effect with Ga(III) on P. aeruginosa, and low cytotoxicity to mammalian cells. The metal coordination for the most promising ligand, 2-Oxo-2-[N-(2,4,6-trihydroxy-benzylidene)-hydrazino]-acetamide (ME0163) with Ga(III) was investigated using extended X-ray absorption fine structure spectroscopy as well as density functional theory. The results showed that Ga(III) chelates the hydrazone with 5- and 6-membered chelating rings, and that the Ga(III)-ME0163 complex enhanced the antibiofilm effect of Ga(III) while suppressing the type three secretion system in P. aeruginosa. The latter effect was not observed for the hydrazone alone and was similar for Ga(III)-citrate and Ga(III)-ME0163 complexes, indicating that the inhibition of virulence was caused by Ga(III).

  • 246.
    Rönmark, Eva
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. The OLIN Studies, Department of Medicine, Sunderby Central Hospital of Norrbotten, Luleå, Sweden.
    Bjerg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. The OLIN Studies, Department of Medicine, Sunderby Central Hospital of Norrbotten, Luleå, Sweden.
    Hedman, L
    Perzanowski, M
    Sundberg, S
    Lundbäck, B
    The Obstructive Lung Disease in Northern Sweden (OLIN) longitudinal paediatric study I: the first 10 years2008In: Clinical Respiratory Journal, ISSN 1752-6981, E-ISSN 1752-699X, Vol. 2, no Suppl 1, p. 26-33Article in journal (Refereed)
    Abstract [en]

    Background: Prospective studies of asthma and allergic conditions based oil the general population are scare.

    Aim: To summarize the methods and main results from a prospective study among school children.

    Methods: In 1996, a cohort of 3525 children aged 7/8 years in Northern Sweden were invited to a questionnaire survey using an expanded ISAAC protocol, and 97% participated. The cohort has been followed up yearly with high participation rate. Skin prick tests were conducted 1996, 2000 and 2006/2007. Allergens in dust from homes and schools have been analyzed. Sub samples have participated in interviews, lung function tests, bronchial hyper reactivity test, and analyses of IgE and IgG antibodies in serum.

    Results: The prevalence of asthma was 6% at age 7-8 years and increased by age. The incidence of physician-diagnosed asthma after the age of 7-8 years was around 1/100/year. The prevalence of positive skin prick test increased from 21% at age 7-8 to 30% at age 11-12 years. Remission of allergic sensitization was rare, while asthma remission was 5% yearly. The main risk factor for asthma and allergic sensitization increased in importance with increasing age. Allergic and non-allergic asthma had different risk factor pattern. Environmental risk factors decreased in impact after the age of 7. Avoidance of pets at home did not protect from asthma or allergic sensitization.

    Conclusion: The study includes important sources of data for further longitudinal analyses that will contribute to the understanding of the development and the nature of asthma and allergic sensitization.

  • 247. Saglani, S
    et al.
    Molyneux, C
    Gong, H
    Rogers, A
    Malmström, K
    Pelkonen, A
    Mäkelä, M
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Bush, A
    Payne, D N R
    Jeffery, P K
    Ultrastructure of the reticular basement membrane in asthmatic adults, children and infants.2006In: Eur Respir J, ISSN 0903-1936, Vol. 28, no 3, p. 505-12Article in journal (Refereed)
  • 248.
    Sahlin, Carin
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    Sleep apnea and sleep: diagnostic aspects2009Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Background: Patients with sleep apnea have frequent apneas and hypopneas during sleep. Apneas can be either central or obstructive. The apnea-hypopnea index (AHI) is the mean number of apneas and hypopneas per hour of sleep.

    Aims: 1) To evaluate the effect of a mandibular advancement device on obstructive apneas and sleep; 2) to evaluate the influence of body position on central apnea frequency; 3) to investigate whether obstructive or central apnea is related to mortality in patients with stroke; and 4) to investigate sleep and sleeping positions in women.

    Methods: Subjects were investigated during whole-night sleep respiratory recordings, either polysomnography including continuous recordings of EEG, EOG, EMG, airflow, respiratory effort, ECG, pulse oximetry and body position, or simplified sleep apnea recordings without EEG, EOG and EMG.

    Results: The frequency of obstructive apneas, hypopneas and arousals decreased and rapid eye movement (REM) sleep increased in patients with mild, moderate and severe sleep apnea during treatment with a mandibular advancement device.

    Central apneas were more prevalent in the supine position compared with the non-supine position in patients with Cheyne-Stokes respiration. The mean ± SD central AHI was 41 ± 13 in the supine position and 26 ± 12 in the non-supine position, p<0.001.

    Stroke patients with obstructive sleep apnea ran an increased risk of death during 10 ± 0.6 years of follow-up with an adjusted hazard ratio of 1.76 (95% CI 1.05-2.95) compared with controls, independent of hypertension, age, body mass index, gender, smoking, diabetes mellitus, atrial fibrillation, Mini-Mental State Examination and Barthel-ADL. Central apnea was not related to early death.

    Total sleep time, sleep efficiency, rapid eye movement sleep, slow wave and time in the supine position decreased with age in women. Sleep quality in women was reduced with age, body mass index, obstructive sleep apnea, smoking, alcohol and hypertension.

    Conclusions: Obstructive sleep apneas and arousals are reduced and REM sleep is increased using a mandibular advancement device in patients with mild, moderate and severe sleep apnea. The frequency of central apneas and hypopneas is increased in the supine position in patients with Cheyne-Stokes respiration. Stroke patients with obstructive sleep apnea run an increased risk of early death. Central sleep apnea was not related to early death among the present patients. Normal values for sleep stages and sleeping positions are presented in a population-based sample of women. Age, body mass index, obstructive sleep apnea, smoking, alcohol and hypertension reduce sleep quality in women.

  • 249.
    Sahlin, Carin
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Franklin, Karl
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Lindberg, Eva
    Institutionen för medicinska vetenskaper, lungmedicin och allergi, Uppsala Universitet.
    Sleep in women: normal values for sleep stages and position and the effect of age, obesity, sleep apnea, smoking, alcohol and hypertension2009In: Sleep Medicine, ISSN 1389-9457, E-ISSN 1878-5506, Vol. 123, no 10, p. 1025-1030Article in journal (Refereed)
    Abstract [en]

    Objectives: To define normal values for total sleep time, sleep latency, sleep efficiency, sleep stages and sleeping positions in women and to investigate how sleep is affected by age, obesity, sleep apnea, smoking, alcohol dependency and hypertension.

    Methods: In a population-based study, 400 Swedish women aged 20-70 years were investigated using overnight in-home polysomnography.

    Results: The mean normal total sleep time was 392 minutes, sleep latency 22 minutes and sleep efficiency 82%. Women spent 31 minutes in sleep stage 1, 244 minutes in stage 2, 41 minutes in stage 3-4 and 76 minutes in rapid eye movement (REM) sleep. They spent 41% of their sleep time in the supine position, 50% in the lateral position and 9% in the prone position. Multivariate analyses revealed that sleep efficiency was lower in older women and in women with hypertension. Sleep latency was short in women with severe sleep apnea and long in smokers, alcohol-dependent and hypertensive women. Total sleep time was long in severe sleep apnea. Sleep stage 3-4 was inversely related to age and body-mass index. Less REM sleep occurred in alcohol-dependent women. Women younger than 45 years old slept a mean of 42% in the lateral position while women of 45 years and older slept 57% in the lateral position (p<0.001).

    Conclusions: In this population-based study of women, we present normal values for sleep stages and sleeping position. We conclude that age, body-mass index, obstructive sleep apnea, smoking, alcohol and hypertension reduce sleep quality. With age, women spend more time sleeping in the lateral position.

  • 250.
    Sahlin, Carin
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandberg, Olov
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine.
    Gustafson, Yngve
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine.
    Bucht, Gösta
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Franklin, Karl
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Obstructive sleep apnea is a risk factor for death in patients with stroke: a 10-year follow-up2008In: Archives of Internal Medicine, ISSN 0003-9926, E-ISSN 1538-3679, Vol. 168, no 3, p. 297-301Article in journal (Refereed)
    Abstract [en]

     

    Background: Sleep apnea occurs frequently among stroke patients, but it is still unknown whether a diagnosis of sleep apnea is an independent risk factor for mortality. We aimed to investigate whether obstructive or central sleep apnea was related to a reduced long-term survival among stroke patients.

    Methods: One hundred and thirty-two of 151 patients admitted for in-hospital stroke rehabilitation in the catchment area of Umeå from 1 April 1995 to 1 May 1997 underwent overnight sleep apnea recordings at 23 ± 8 days after onset of stroke. All patients were followed-up prospectively for a mean (SD) of 10.0 ± 0.6 years, with death as the primary outcome and no one was lost to follow-up. Obstructive sleep apnea was defined when the obstructive apnea-hypopnea index was over 15 and central sleep apnea when the central apnea-hypopnea index was over 15. Patients with an obstructive and a central apnea-hypopnea index below 15 served as controls.

    Results: Of 132 enrolled patients, 116 had died at follow-up. The risk of death was higher among the 23 patients with obstructive sleep apnea than controls (adjusted hazard ratio, 1.76; 95% confidence interval 1.05 to 2.95, p=0.03), independent of age, gender, body-mass index, smoking, hypertension, diabetes mellitus, atrial fibrillation, mini-mental state examination and Barthel activity of daily living There was no difference in mortality between the 28 patients with central sleep apnea and controls (adjusted hazard ratio, 1.07; 95 percent confidence interval 0.65 to 1.76, p=0.053).

    Conclusions: Stroke patients with obstructive sleep apnea run an increased risk of early death. Central sleep apnea was not related to early death among the present patients.

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  • text
  • asciidoc
  • rtf