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Träfflista för sökning "WFRF:(Nielsen Jörn) ;pers:(Broberg Karin)"

Sökning: WFRF:(Nielsen Jörn) > Broberg Karin

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  • Jönsson, Lena S, et al. (författare)
  • Gene expression analysis in induced sputum from welders with and without airway-related symptoms.
  • 2011
  • Ingår i: International Archives of Occupational and Environmental Health. - : Springer Science and Business Media LLC. - 1432-1246 .- 0340-0131. ; Okt, s. 105-113
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To identify changes in gene expression in the airways among welders, with and without lower airway symptoms, working in black steel. METHODS: Included were 25 male, non-smoking welders. Each welder was sampled twice; before exposure (after vacation), and after 1 month of exposure. From the welders (14 symptomatic, of whom 7 had asthma-like symptoms), RNA from induced sputum was obtained for gene expression analysis. Messenger RNA from a subset of the samples (n = 7) was analysed with microarray technology to identify genes of interest. These genes were further analysed using quantitative PCR (qPCR; n = 22). RESULTS: By comparing samples before and after exposure, the microarray analysis resulted in several functional annotation clusters: the one with the highest enrichment score contained "response to wounding", "inflammatory response" and "defence response". Seven genes were analysed by qPCR: granulocyte colony-stimulating factor 3 receptor (CSF3R), superoxide dismutase 2, interleukin 8, glutathione S-transferase pi 1, tumour necrosis factor alpha-induced protein 6 (TNFAIP6), interleukin 1 receptor type II and matrix metallopeptidase 25 (MMP25). Increased levels of CSF3R, TNFAIP6 and MMP25 were indicated among asthmatic subjects compared to non-symptomatic subjects, although the differences did not reach significance. CONCLUSIONS: Workers' exposure to welding fumes changed gene expression in the lower airways in genes involved in inflammatory and defence response. Thus, microarray and qPCR technique can demonstrate markers of exposure to welding fumes and possible disease-related markers. However, further studies are needed to verify genes involved and to further characterise the mechanism for welding fumes-associated lower airway symptoms.
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  • Jönsson, Lena S, et al. (författare)
  • Gene expression in nasal lavage from hairdressers exposed to persulphate.
  • 2009
  • Ingår i: International Archives of Occupational and Environmental Health. - : Springer Science and Business Media LLC. - 1432-1246 .- 0340-0131. ; 82, s. 1261-1266
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: Many hairdressers experience work-related symptoms from the airways caused by bleaching powder. This contains persulphates, which could be irritating to the mucous membrane and also may evoke an allergic reaction. However, specific IgE antibodies are difficult to detect. We found earlier that hairdressers with work-related bleaching powder-associated nasal symptoms reacted to persulphate, but that atopics also did and that the mechanism appeared to be similar in the two groups. In this study, we analysed gene expression of cytokines in the nose in order to further investigate the mechanism for work-related bleaching powder-associated nasal symptoms. METHODS: The study subjects belonged to either hairdressers with work-related bleaching powder-associated nasal symptoms (S; n = 6), hairdressers without work-related bleaching powder-associated symptoms (WS; n = 7) or atopics (A; n = 6). Nasal lavage was performed before and during (up to 4 h after the last challenge) provocation with potassium persulphate. Expression of two genes involved in allergic inflammation [interleukin 5 (IL5) and IL13] and one involved in cell-mediated immunity (interferon-gamma; IFNG) were analysed in nasal lavage with quantitative PCR. RESULTS: The change of IL5 in the S group differed when compared to the WS group (P = 0.0051), in the A group when compared to the WS group (P = 0.014), but not in the S group when compared to the A group (P = 0.82). The change of IL13 in the A group differed when compared to the S (P = 0.041) and WS (P = 0.014) groups, but no difference was noticed between the S and WS groups (P = 0.30). The relative level of IFNG increased from before challenge to during challenge in the S group (P = 0.031). CONCLUSIONS: Symptomatic hairdressers showed increased expression of IL5 and IFNG, but not IL13, during challenge. Hairdressers without work-related bleaching powder-associated nasal symptoms showed no markedly changed reaction. Atopics showed increased expression of IL5 and IL13. Thus, this may indicate a difference in the mechanism of symptoms between symptomatic hairdressers and atopics. However, due to the low number of participants, further studies are needed to elucidate the mechanism for persulphate-associated nasal symptoms.
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7.
  • Krais, Annette M., et al. (författare)
  • Biomarkers after Controlled Inhalation Exposure to Exhaust from Hydrogenated Vegetable Oil (HVO)
  • 2021
  • Ingår i: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1661-7827 .- 1660-4601. ; 18:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Hydrogenated vegetable oil (HVO) is a renewable diesel fuel used to replace petroleum diesel. The organic compounds in HVO are poorly characterized; therefore, toxicological properties could be different from petroleum diesel exhaust. The aim of this study was to evaluate the exposure and effective biomarkers in 18 individuals after short-term (3 h) exposure to HVO exhaust and petroleum diesel exhaust fumes. Liquid chromatography tandem mass spectrometry was used to analyze urinary biomarkers. A proximity extension assay was used for the measurement of inflammatory proteins in plasma samples. Short-term (3 h) exposure to HVO exhaust (PM1 ~1 µg/m3 and ~90 µg/m3 for vehicles with and without exhaust aftertreatment systems, respectively) did not increase any exposure biomarker, whereas petroleum diesel exhaust (PM1 ~300 µg/m3 ) increased urinary 4-MHA, a biomarker for p-xylene. HVO exhaust from the vehicle without exhaust aftertreatment system increased urinary 4-HNE-MA, a biomarker for lipid peroxidation, from 64 ng/mL urine (before exposure) to 141 ng/mL (24 h after exposure, p < 0.001). There was no differential expression of plasma inflammatory proteins between the HVO exhaust and control exposure group. In conclusion, short-term exposure to low concentrations of HVO exhaust did not increase urinary exposure biomarkers, but caused a slight increase in lipid peroxidation associated with the particle fraction.
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