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Träfflista för sökning "L773:1399 3003 OR L773:0903 1936 ;srt2:(2005-2009)"

Sökning: L773:1399 3003 OR L773:0903 1936 > (2005-2009)

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61.
  • Pellegrino, R, et al. (författare)
  • Interpretative strategies for lung function tests.
  • 2005
  • Ingår i: The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology. - : European Respiratory Society (ERS). - 0903-1936. ; 26:5, s. 948-68
  • Tidskriftsartikel (refereegranskat)
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62.
  • Persson, H L, et al. (författare)
  • Lysosomal iron in pulmonary alveolar proteinosis : a case report.
  • 2009
  • Ingår i: The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology. - : European Respiratory Society (ERS). - 1399-3003. ; 33:3, s. 673-679
  • Tidskriftsartikel (refereegranskat)abstract
    • Pulmonary alveolar proteinosis is characterised by accumulation of surfactant-like material in the distal air spaces. Since lysosomes play a crucial role for degradation of large biomolecules taken up from the cell's environment, it was hypothesised that oxidant-induced lysosomal disruption and ensuing cell death might play a role in disease development. In the present study, alveolar macrophages, harvested by whole-lung lavage from a patient diagnosed with pulmonary alveolar proteinosis, are shown to contain large amounts of undigested material within lysosomes, and the same organelle exhibits increased amounts of haemosiderin-bound iron. Compared with murine macrophage-like J774 cells (iron exposed or not), the status of human macrophages was pro-oxidative, i.e. macrophages exhibited a low level of the antioxidant glutathione and large amounts of iron available for Fenton-type chemistry. As a consequence, macrophageal lysosomes were particularly fragile when exposed to physiological concentrations of hydrogen peroxide (generated by glucose oxidase in culture medium). Such lysosomal disruption resulted in extensive cell death by both necrosis and apoptosis independent of caspase-3 activation. Considering the potential role of iron-catalysed oxidant-induced lysosomal rupture and ensuing cell killing for pulmonary alveolar proteinosis pathology and disease progression, whole-lung lavage might be considered early in those cases in which cytochemical staining reveals great numbers of haemosiderin-laden alveolar macrophages.
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63.
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64.
  • Rocklöv, Joacim, 1979-, et al. (författare)
  • Winter mortality modifies the heat-mortality association the following summer
  • 2009
  • Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 33:2, s. 245-251
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study aimed to investigate how the heat-related increase in deaths in summer and the extent of mortality displacement depend on influenza and other categories of mortality in the previous winter, which when low leaves a greater pool of susceptible individuals. Mortality data from Stockholm, Sweden, from 1990-2002 were stratified into a summer period and a winter period. A Poisson regression model was established for the daily mortality in the summer, with temperature and confounders as explanatory variables. In addition, indicators of total, respiratory, cardiovascular and influenza mortality of the winter period were incorporated as effect modifiers in the summer model, and lagged effects in strata defined by indicators were studied. A high rate of respiratory as well as cardiovascular mortality in winter reduced the heat effect the following summer, and influenza mortality tended to do so as well. The cumulative effect per degrees C increase was 0.95% below and 0.89% above a threshold (21.3 degrees C) after a winter with low cardiovascular and respiratory mortality, but -0.23% below and 0.21% above the threshold after a winter with high cardiovascular and respiratory mortality. The current study shows that high respiratory, cardiovascular and influenza mortality in winter leads to lower temperature effects in the following summer. It also suggests that persons for whom influenza may be fatal are often also susceptible to heat and this subgroup might, therefore, not benefit as much as expected from influenza vaccinations.
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65.
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66.
  • Rydell-Törmänen, Kristina, et al. (författare)
  • Direct evidence of secondary necrosis of neutrophils during intense lung inflammation.
  • 2006
  • Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 1399-3003 .- 0903-1936. ; 28:2, s. 268-274
  • Tidskriftsartikel (refereegranskat)abstract
    • Several pulmonary inflammatory conditions are characterised by infiltration of neutrophils. Normally, neutrophils are silently removed by apoptosis, followed by phagocytosis. However, if phagocytosis fails, apoptotic cells undergo secondary necrosis. Recent findings of increased levels of the pan-necrosis marker lactate dehydrogenase in bronchoalveolar lavage from lipopolysaccharide-exposed mice implies potential involvement of secondary necrosis. Using a similar model, this study aimed to identify the source of lactate dehydrogenase and to search for direct histological evidence of secondary necrosis. Lipopolysaccharide (LPS) was administered to the lungs of BALB/c mice, and bronchoalveolar lavage and tissue samples were collected 4, 12, 24, 36, 48, 60 and 72 h after administration. LPS induced a patchy neutrophil-rich lung inflammation, where the numbers of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling-positive neutrophils were increased at 12 h and onwards. Lavage levels of neutrophils and lactate dehydrogenase increased significantly at 4 and 24 h, respectively. Detailed electron microscopic assessment of neutrophil activation and death modes revealed that up to 14% of the neutrophils were undergoing secondary necrosis, whereas apoptotic or primary necrotic structural cells were rarely found. In summary, this study provides direct evidence that secondary necrosis of neutrophils is a common process during intense lung inflammation. This implies that neutrophil apoptosis may cause rather than resolve airway inflammation.
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67.
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68.
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69.
  • Sahlin, Carin, 1953-, et al. (författare)
  • Cheyne-Stokes respiration and supine dependency
  • 2005
  • Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 25:5, s. 829-33
  • Tidskriftsartikel (refereegranskat)
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70.
  • Samoli, E, et al. (författare)
  • Short-term effects of nitrogen dioxide on mortality : an analysis within the APHEA project
  • 2006
  • Ingår i: European Respiratory Journal. - Copenhagen : Munksgaard. - 0903-1936 .- 1399-3003. ; 27:6, s. 1129-1138
  • Tidskriftsartikel (refereegranskat)abstract
    • The short-term effects of nitrogen dioxide (NO2) on total, cardiovascular and respiratory mortality in 30 European cities participating in the Air Pollution on Health: a European Approach (APHEA)-2 project were investigated. The association was examined using hierarchical models implemented in two stages. In the first stage, data from each city were analysed separately, whereas in the second stage, the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity. A significant association of NO2 with total, cardiovascular and respiratory mortality was found, with stronger effects on cause-specific mortality. There was evidence of confounding in respiratory mortality with black smoke and sulphur dioxide. The effect of NO2 on total and cardiovascular mortality was observed mainly in western and southern European cities, and was larger when smoking prevalence was lower and household gas consumption was higher. The effect of NO2 on respiratory mortality was higher in cities with a larger proportion of elderly persons in the population and higher levels of particulate matter with a 50% cut-off aerodynamic diameter of 10 μm. The results of this large study are consistent with an independent effect of nitrogen dioxide on mortality, but the role of nitrogen dioxide as a surrogate of other unmeasured pollutants cannot be completely ruled out.
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