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- Gidhagen, L, et al.
(author)
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Model simulation of ultrafine particles inside a road tunnel
- 2003
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In: Atmospheric Environment. - 1352-2310. ; 37:15, s. 2023-2036
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Journal article (peer-reviewed)abstract
- A monodispersive aerosol dynamic model, coupled to a 3D hydrodynamical grid model, has been used to study the dynamics of ultrafine particles inside a road tunnel in Stockholm, Sweden. The model results were compared to measured data of particle number concentrations, traffic intensity and tunnel ventilation rate. Coagulation and depositional losses to the tunnel walls were shown to be important processes during traffic peak hours, together contributing to losses of 77% of the particles smaller than 10nm and 41% of the particles of size 10-29nm. Particle growth due to water uptake or the presence of a micron-sized, resuspended particle fraction did not have any significant effect on the number of particles lost due to coagulation. Model simulation of particle number concentration response to temporal variations in traffic flow showed that constant emission factors could be used to reproduce the concentration variations of the particles larger than 29nm, while vehicle-speed-dependent factors are suggested to reproduce the variation of the smallest fractions. The emission factors for particle number concentrations estimated from the model simulation are in general higher and show a larger contribution from light-duty vehicles than what has been reported from a tunnel in California. The model study shows that combined measurements and model simulations in road tunnels can be used to improve the determinations of vehicle emission factors for ultrafine particles under realistic driving conditions. (C) 2003 Elsevier Science Ltd. All rights reserved.
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- Masocha, W, et al.
(author)
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Cerebral vessel laminins and IFN-gamma y define Trypanosoma brucei brucei penetration of the blood-brain barrier
- 2004
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In: Journal of Clinical Investigation. - 0021-9738. ; 114:5, s. 689-694
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Journal article (peer-reviewed)abstract
- Subspecies of Trypanosoma brucei cause severe brain diseases after penetration of the blood-brain barrier. We investigated whether cytokines that modulate inflammatory cell infiltration into the brain also influence T. brucei neuroinvasion. Migration of a rodent pathogenic T. brucei strain from the cerebral blood vessels into the brain parenchyma was impeded in IFN-gamma(-/-), IFN-gamma receptor(-/-) (IFN-gammaR(-/-)), IL-12p40(-/-), and recombinant activating gene-1(-/-) (RAG-1(-/-)) mice as compared with their WT littermates despite higher levels of parasitemia in the mutant strains. Parasites accumulated in the perivascular compartment, confined between the endothelial and the parenchymal basement membranes, in certain areas of the brains of IFN-gamma(-/-), IFN-gammaR(-/-), and RAG-1(-/-) mice. This accumulation occurred around endothelial basement membranes containing the laminin alpha4 chain, while blood vessels showing robust laminin alpha5 chain immunostaining were not associated with parasite infiltration. The number of CD4(+) and CD8(+) T cells infiltrating the brain parenchyma was also reduced in the IFN-gamma(-/-) and IFN-gammaR(-/-) mice. Our findings suggest that lymphocyte-derived IFN-gamma facilitates trypanosome penetration across cerebral blood vessels and that the site of penetration is determined by the composition of the basement membranes of these vessels.
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