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The challenge of obtaining correct data for cellular release of inflammatory mediators after in vitro exposure to particulate matter.Pulmonary phthalate exposure and asthma - is PPAR a plausible mechanistic link?Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines.Health effects of residential wood smoke particles: the importance of combustion conditions and physicochemical particle propertiesBisphenol A Is More Potent than Phthalate Metabolites in Reducing Pancreatic β-Cell Function.Cytokine responses induced by diesel exhaust particles are suppressed by PAR-2 silencing and antioxidant treatment, and driven by polar and non-polar soluble constituents.The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles.Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7.Mono-2-ethylhexylphthalate (MEHP) induces TNF-α release and macrophage differentiation through different signalling pathways in RAW264.7 cells.Differential effects of the particle core and organic extract of diesel exhaust particles.Early life exposure to bisphenol A investigated in mouse models of airway allergy, food allergy and oral tolerance.Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice.Transmaternal bisphenol A exposure accelerates diabetes type 1 development in NOD mice.Long-term bisphenol A exposure accelerates insulitis development in diabetes-prone NOD mice.
P50
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P50
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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Anette Kocbach Bølling
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