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Oxidative stress and apoptosis are induced in human endothelial cells exposed to urban particulate matter.
TLDR
The activation of HUVEC induced by PM(2.5) and PM(10) is related with an oxidative stress, suggesting that these particles may participate in the development of cardiovascular and inflammatory diseases. Expand
TiO₂ nanoparticles induce dysfunction and activation of human endothelial cells.
TLDR
TiO₂ induced HUVEC activation, inhibition of cell proliferation with increased cell death, and oxidative stress, which were associated with oxidative stress and NF-κB pathway activation. Expand
PM2.5 and PM10 Induce the Expression of Adhesion Molecules and the Adhesion of Monocytic Cells to Human Umbilical Vein Endothelial Cells
TLDR
PM2.5 and PM10 induce the activation of HUVEC, leading to monocytic adhesion via the expression of adhesion molecules, suggesting that these particles may participate in the development of inflammatory diseases. Expand
Multiple Molecular Targets Associated with Genomic Instability in Lung Cancer
TLDR
A current outlook of the connection between LC and genomic instability at the molecular and clinical level is presented summarizing its implications for diagnosis, therapy, and prognosis. Expand
Curcumin inhibits activation induced by urban particulate material or titanium dioxide nanoparticles in primary human endothelial cells
TLDR
The results suggest an anti-inflammatory and antioxidant role by curcumin attenuating the activation caused on endothelial cells by exposure to particles and could be useful in the treatment of diseases where an inflammatory process and endothelial activation are involved. Expand
E-Selectin expression in human endothelial cells exposed to PM10: the role of endotoxin and insoluble fraction.
TLDR
In conclusion, PM10 induces endothelial cell activation, evidenced by enhanced E-Selectin expression, manifested functionally as an increase in monocytic cell adhesion. Expand
TiO2 nanoparticles induce endothelial cell activation in a pneumocyte-endothelial co-culture model.
TLDR
An in vitro model that mimics the alveolar-capillary interface and challenges the model using TiO nanoparticles indicate that exposing pneumocytes to TiO-NPs causes endothelial cell activation. Expand
Dehydroepiandrosterone inhibits the activation and dysfunction of endothelial cells induced by high glucose concentration
TLDR
It is suggested that D HEA protects against the activation of endothelial cells induced by high concentrations of glucose, indicating that DHEA could be useful in the treatment of hyperglycemia and diabetes. Expand
Vanadium pentoxide induces activation and death of endothelial cells
TLDR
Vanadium pentoxide induced serious endothelial cell damage, probably related to the increased cardiovascular morbidity and mortality observed in individuals living in highly air‐polluted areas. Expand
Dehydroepiandrosterone Protects Endothelial Cells against Inflammatory Events Induced by Urban Particulate Matter and Titanium Dioxide Nanoparticles
TLDR
DHEA exerts significant anti-inflammatory and antioxidative effects on the damage induced by particles in HUVEC, suggesting that DHEA could be useful to counteract the harmful effects and inflammatory diseases induced by PM and NPs. Expand
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