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Translocation of Inhaled Ultrafine Manganese Oxide Particles to the Central Nervous System
TLDR
The olfactory neuronal pathway is efficient for translocating inhaled Mn oxide as solid UFPs to the central nervous system and that this can result in inflammatory changes. Expand
Role of the alveolar macrophage in lung injury: studies with ultrafine particles.
TLDR
The dual role of AM for modifying particle-induced lung injury is demonstrated, both preventing such injury and contributing to it, and the increased pulmonary toxicity of ultrafine particles is related to their larger surface area and to their increased interstitial access. Expand
Effects of subchronically inhaled carbon black in three species. I. Retention kinetics, lung inflammation, and histopathology.
TLDR
Lung inflammation and histopathology were more severe and prolonged in rats than in mice and hamsters, and both were similar in rats exposed to mid-dose HSCb and LSCb, showing that hamsters have the most efficient clearance mechanisms and least severe responses of the three species. Expand
A perpetual cascade of cytokines postirradiation leads to pulmonary fibrosis.
TLDR
The temporal relationship between the elevation of specific cytokines and the histological and biochemical evidence of fibrosis serves to illustrate the continuum of response, which, it is believed, underlies pulmonary radiation reactions and supports the concept of a perpetual cascade of cytokines produced immediately after irradiation. Expand
Acute pulmonary effects of ultrafine particles in rats and mice.
TLDR
Evaluating pulmonary effects induced in rats and mice by ultrafine particles of known high toxicity in order to obtain information on principles of ultrafine particle toxicology found that the pulmonary toxicity of the ultrafine Teflon fumes could be prevented by adapting the animals with short 5-minute exposures on 3 days prior to a 15-minute exposure. Expand
Pulmonary chemokine and mutagenic responses in rats after subchronic inhalation of amorphous and crystalline silica.
TLDR
The observation that genotoxic effects in alveolar epithelial cells occurred only after crystalline but not amorphous silica exposure, despite a high degree of inflammatory-cell response after subchronic exposure to both types of silica, suggests that in addition to an inflammatory response, particle biopersistence, solubility, and direct or indirect epithelial cell cytotoxicity may be key factors for the induction of either mutagenic events or target cell death. Expand
Radiation pneumonitis and early circulatory cytokine markers.
TLDR
Analysis of a panel of circulating cytokines with different putative functions in radiation pulmonary injury identified IL-1alpha and IL-6 as early circulating cytokine markers for radiation pneumonitis. Expand
The influence of protein adsorption on nanoparticle association with cultured endothelial cells.
TLDR
It is concluded that cellular association is not dependent on the identity of adsorbed proteins and therefore unlikely to require specific binding to any particular cellular receptors. Expand
Extracellular glutathione peroxidase in human lung epithelial lining fluid and in lung cells.
TLDR
It is concluded that more than half of GPx activity in BAL is due to e GPx, and that BEC, AM, and interstitial cells are potential sources of pulmonary eGPx. Expand
A Comparative Dose-Related Response of Several Key Pro- and Antiinflammatory Mediators in the Lungs of Rats, Mice, and Hamsters After Subchronic Inhalation of Carbon Black
TLDR
Investigating mechanisms underlying species specificity in particle-induced lung inflammation found greater propensity for generating a proinflammatory response, whereas mice and hamsters demonstrated an increased antiinflammatory response. Expand
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