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Mechanisms linking traffic-related air pollution and atherosclerosisTissue biodistribution of intravenously administrated titanium dioxide nanoparticles revealed blood-brain barrier clearance and brain inflammation in ratEngine exhaust particulate and gas phase contributions to vascular toxicityInhaled diesel emissions alter atherosclerotic plaque composition in ApoE(-/-) miceVehicular emissions induce vascular MMP-9 expression and activity associated with endothelin-1-mediated pathwaysA comparison of vascular effects from complex and individual air pollutants indicates a role for monoxide gases and volatile hydrocarbons.Identification of chemical components of combustion emissions that affect pro-atherosclerotic vascular responses in mice.Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.Exposure to vehicle emissions results in altered blood brain barrier permeability and expression of matrix metalloproteinases and tight junction proteins in mice.Loss of the aryl hydrocarbon receptor induces hypoxemia, endothelin-1, and systemic hypertension at modest altitude.Cardiopulmonary response to inhalation of biogenic secondary organic aerosol.The effects of α-pinene versus toluene-derived secondary organic aerosol exposure on the expression of markers associated with vascular disease.Insulin regulation in AhR-null mice: embryonic cardiac enlargement, neonatal macrosomia, and altered insulin regulation and response in pregnant and aging AhR-null females.Endothelin-1-mediated increase in reactive oxygen species and NADPH Oxidase activity in hearts of aryl hydrocarbon receptor (AhR) null mice.The National Environmental Respiratory Center (NERC) experiment in multi-pollutant air quality health research: IV. Vascular effects of repeated inhalation exposure to a mixture of five inorganic gases.Gasoline exhaust emissions induce vascular remodeling pathways involved in atherosclerosis.The National Environmental Respiratory Center (NERC) experiment in multi-pollutant air quality health research: II. Comparison of responses to diesel and gasoline engine exhausts, hardwood smoke and simulated downwind coal emissions.Cardiopulmonary response to inhalation of secondary organic aerosol derived from gas-phase oxidation of tolueneDiesel exhaust exposure enhances venoconstriction via uncoupling of eNOSCharacterizing the role of endothelin-1 in the progression of cardiac hypertrophy in aryl hydrocarbon receptor (AhR) null mice
P50
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P50
description
hulumtuese
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Amie Lund
@ast
Amie Lund
@en
Amie Lund
@es
Amie Lund
@nl
type
label
Amie Lund
@ast
Amie Lund
@en
Amie Lund
@es
Amie Lund
@nl
prefLabel
Amie Lund
@ast
Amie Lund
@en
Amie Lund
@es
Amie Lund
@nl
P1053
L-4355-2017
P106
P21
P31
P3829
P496
0000-0002-0878-751X