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Sökning: WFRF:(Westman Ola)

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1.
  • Engwall, Magnus, 1965-, et al. (författare)
  • Polycyclic aromatic hydrocarbons (PAHs) reduce hepatic beta-oxidation of fatty acids in chick embryos
  • 2013
  • Ingår i: Environmental Science and Pollution Research. - : Springer Science and Business Media LLC. - 0944-1344 .- 1614-7499. ; 20:3, s. 1881-1888
  • Tidskriftsartikel (refereegranskat)abstract
    • Polycyclic aromatic hydrocarbons (PAHs) are widespread fused-ring contaminants formed during incomplete combustion of almost all kind of organic materials from both natural and anthropogenic sources. Some PAHs have been shown to be carcinogenic to humans, and a wide range of PAHs are found in wildlife all around the globe including avian species. The purpose of this project was to assess the effects of a standard mixture of 16 PAHs (United States Environmental Protection Agency) on the hepatic fatty acid beta-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The hepatic beta-oxidation was measured using a tritium release assay with [9,10-H-3]-palmitic acid (16:0) as substrate. Treated groups were divided into groups of 0.05, 0.1, 0.3, 0.5, and 0.8 mg PAHs/kg egg weight. The hepatic beta-oxidation was reduced after exposure in ovo to the 16 PAHs mixture compared to control. The mechanisms causing reduced fatty acid oxidation in the present study are unclear, however may be due to deficient membrane structure, the functionality of enzymes controlling the rate of fatty acid entering into the mitochondria, or complex pathways connected to endocrine disruption. To the best of our knowledge, this is the first time a PAH-caused reduction of hepatic beta-oxidation of fatty acids in avian embryos has been observed. The implication of this finding on risk assessment of PAH exposure in avian wildlife remains to be determined.
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2.
  • Goel, Suchi, et al. (författare)
  • RIFINs are adhesins implicated in severe Plasmodium falciparum malaria
  • 2015
  • Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 21:4, s. 314-317
  • Tidskriftsartikel (refereegranskat)abstract
    • Rosetting is a virulent Plasmodium falciparum phenomenon associated with severe malaria. Here we demonstrate that P. falciparum-encoded repetitive interspersed families of polypeptides (RIFINs) are expressed on the surface of infected red blood cells (iRBCs), bind to RBCs-preferentially of blood group A-to form large rosettes and mediate microvascular binding of iRBCs. We suggest that RIFINs have a fundamental role in the development of severe malaria and thereby contribute to the varying global distribution of ABO blood groups in the human population.
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  • Nordén, Marcus, 1982-, et al. (författare)
  • Perfluorooctane sulfonate increases β-oxidation of palmitic acid in chicken liver
  • 2012
  • Ingår i: Environmental Science and Pollution Research. - Heidelberg, Germany : Springer Berlin/Heidelberg. - 0944-1344 .- 1614-7499. ; 19:5, s. 1859-1863
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: Perfluorooctane sulfonate (PFOS) belongs to a group of chemicals called perfluoroalkyl acids that have been extensively used in various applications such as stain and oil resistant treatments for fabrics, fire-fighting foams, and insecticides. These chemicals present an environmental and health risk being present in many samples both in wildlife and humans. In this study, we investigate the effect of PFOS on fatty acid β-oxidation in developing chicken embryos.Methods: Fertilized chicken eggs were exposed in ovo to PFOS at day 4 of incubation. On day 10, the eggs were dissected and livers were incubated in vitro with (3)H-palmitic acid for 2 h. The media were collected, and after clean up, the amount of tritiated water was measured with liquid scintillation counting to determine the rate of palmitic acid β-oxidation.Results: PFOS was found to induce fatty acid β-oxidation at doses starting from a lowest observed effect level (LOEL) of 0.1 μg/g egg weight. Maximum induction of 77 % compared to control was seen at 0.3 μg/g.Conclusions: The administered doses in which effects are seen are around and even lower than the levels that can be found in wild populations of birds. General population human levels are a factor of two to three times lower than the LOEL value of this study. The environmental contamination of PFOS therefore presents a possibility of effects in wild populations of birds.
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5.
  • Westman, Ola, 1971-, et al. (författare)
  • An oxygenated metabolite of benzo[a]pyrene increases hepatic beta-oxidation of fatty acids in chick embryos
  • 2014
  • Ingår i: Environmental Science and Pollution Research. - Heidelberg : Springer Berlin/Heidelberg. - 0944-1344 .- 1614-7499. ; 21:9, s. 6243-6251
  • Tidskriftsartikel (refereegranskat)abstract
    • Polycyclic aromatic hydrocarbons (PAHs) are well-known carcinogens to humans and ecotoxicological effects have been shown in several studies. However, PAHs can also be oxidized into more water soluble-oxygenated metabolites (Oxy-PAHs). The first purpose of the present project was to (1) assess the effects of a mixture containing three parent PAHs: anthracene, benz[a]anthracene, and benzo[a]pyrene versus a mixture of their oxygenated metabolites, namely: anthracene-9,10-dione, benz[a]anthracene-7,12-dione, and 9,10-dihydrobenzo[a]pyrene-7-(8H)-one on the hepatic fatty acid beta-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The second and also main purpose of the project was to (2) assess the effects of the parent PAHs versus their oxy-PAHs analogues when injected individually, followed by (3) additional testing of the individual oxy-PAHs. The hepatic beta-oxidation was measured using a tritium release assay with [9,10-H-3]-palmitic acid (16:0) as substrate. The result from the first part (1) showed reduced hepatic beta-oxidation after exposure in ovo to a mixture of three PAHs, however, increased after exposure to the mixture of three oxy-PAHs compared to control. The result from the second part (2) and also the follow-up experiment (3) showed that 9,10-dihydrobenzo[a]pyrene-7-(8H)-one was the causative oxy-PAH. The implication of this finding on the risk assessment of PAH metabolite exposure in avian wildlife remains to be determined. To the best of our knowledge, no similar studies have been reported.
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7.
  • Westman, Ola, et al. (författare)
  • Comparative study and characterization of mutagenicity and AhR-agonistic potency of contaminated soil, remediated soil, urban city soil and rural soil
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Current risk assessment of PAH-contaminated soils is usually based on chemical analysis of a small number of PAHs. The use of effect-based methods for risk assessment would yield results covering more of the effect of all the chemicals in the soil. To put such effect based data into context we tested a relative approach in which effects of contaminated soil were compared to clean rural and urban soils. This concept of relative risk assessment was tested by studying the mutagenic and AhR-agonistic potency of contaminated soil and urban soil compared to farm soil from selected ecological farms. A set of 21 soil samples was collected: 11 PAH-contaminated samples (collected in collaboration with three Swedish remediation companies), 5 urban samples (collected in Swedish cities) and 5 soil samples from ecological farms. The urban and rural samples were collected at the surface (0-10 cm deep), the contaminated samples were collected from piles during remediation (100-200 cm deep). To evaluate the toxicants in the soil sample, lipophilic sample extracts were tested in two different assays; (i) the Ames Fluctuation Assay (AFA) mutant strains TA98 and TA100 of Salmonella typhimurium with and without a metabolic activation system (rat-liver homogenate S9) to determine the mutagenic potential of the soil samples and (ii) the cell mechanism-specific H4IIE-luc assay to determine the Ahreceptor (AhR) activating potency of the soil extracts. The results showed clear mutagenicity, both direct and indirect, in one of the PAH-contaminated samples and three other PAH samples also demonstrated some mutagenic activity. The extracts from urban city soil showed mutagenicity in three of the 5 samples, while none of the ecological farm samples had mutagenic extracts. The bio-TEQ values were very high for all remediated samples and elevated in one urban sample. Bio-TEQ values were low in the ecological farm extracts. These findings demonstrate that the present investigation scheme using two different bioassays to determine the mutagenic potential and the Ah receptor activating potency of soil extracts is a suitable method for testing toxic properties of soil extracts. The concept of relative risk assessment using background samples from rural and urban areas and effect based testing shows promise for further development.
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9.
  • Westman, Ola, et al. (författare)
  • Effects of perfluorinated compounds on hepatic fatty acid oxidation in avian embryos using a tritium release assay
  • 2010
  • Ingår i: In Vivo. - : International Institute of Anticancer Research. - 0258-851X .- 1791-7549. ; 24:3, s. 363-364
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Due to high persistence and bioaccumulationperfluorinated compounds (PFCs) are found globally in varioustypes of wildlife samples and also human samples¹. Accordingto our laboratory studies, perfluorooctane sulfonate (PFOS) hascaused early mortality in chicken embryos at doses close toconcentrations found in eggs of the Baltic guillemot². We havedesigned a method in which hepatic embryonic tissue fromchicken (Gallus domesticus) is used to investigate the effectsof PFCs on the β-oxidation of fatty acids.Materials and Methods: The embryos were exposed inovo to PFCs. On day 10 embryo livers were incubated invitro with tritiated fatty acids. Fatty acid oxidation was thencalculated from the tritium released into water, using ascintillation counter.Results: Our studies suggest a small but significant increaseof the β-oxidation of fatty acids in chicken embryonic livertissue in vitro after in ovo exposure to PFOS. The β-oxidationwas significantly induced after embryo exposure to 1 mg/kgPFOS (p=0.003) and 10 mg/kg PFOS (p=0.04), being 39%and 34% higher, respectively compared to control.Conclusion: The results show that in ovo exposure incombination with an in vitro method using a tritium releaseassay to detect effects on the β-oxidation of fatty acids inavian embryo hepatic tissue could be a useful method inelucidating possible mechanisms behind avian developmental toxicity.
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