| 1. |
- Kanai, M, et al.
(författare)
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- 2023
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swepub:Mat__t
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| 2. |
- Niemi, MEK, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 3. |
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| 4. |
- Hale, Sarah E., et al.
(författare)
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Effects of Chemical, Biological, and Physical Aging As Well As Soil Addition on the Sorption of Pyrene to Activated Carbon and Biochar
- 2011
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Ingår i: Environmental Science and Technology. - : American Chemical Society (ACS). - 0013-936X .- 1520-5851. ; 45:24, s. 10445-10453
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Tidskriftsartikel (refereegranskat)abstract
- In this study, the suitability of biochar and activated carbon (AC) for contaminated soil remediation is investigated by determining the sorption of pyrene to both materials in the presence and absence of soil and before as well as after aging. Biochar and AC were aged either alone or mixed with soil via exposure to (a) nutrients and microorganisms (biological), (b) 60 and 110 degrees C (chemical), and (c) freeze-thaw cycles (physical). Before and after aging, the pH, elemental composition, cation exchange capacity (CEC), microporous SA, and sorption isotherms of pyrene were quantified. Aging at 110 degrees C altered the physicochemical properties of all materials to the greatest extent (for example, pH increased by up to three units and CEC by up to 50% for biochar). Logarithmic K(Fr) values ranged from 7.80 to 8.21 (ng kg(-1)) (ng L(-1))(-nF) for AC and 5.22 to 6.21 (ng kg(-1))(ng L(-1))(-nF) for biochar after the various aging regimes. Grinding biochar to a smaller particle size did not significantly affect the sorption of d(10) pyrene, implying that sorption processes operate on the subparticle scale. Chemical aging decreased the sorption of pyrene to the greatest extent (up to 1.8 log unit for the biochar+soil). The sorption to AC was affected more by the presence of soil than the sorption to biochar was. Our results suggest that AC and biochar have a high sorption capacity for pyrene that is maintained both in the presence of soil and during harsh aging. Both materials could therefore be considered in contaminated land remediation.
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| 5. |
- Kia, Richard, et al.
(författare)
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MicroRNA-122 : a novel hepatocyte-enriched in vitro marker of drug-induced cellular toxicity
- 2015
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Ingår i: Toxicological Sciences. - : Oxford University Press. - 1096-6080 .- 1096-0929. ; 144:1, s. 173-185
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Tidskriftsartikel (refereegranskat)abstract
- Emerging hepatic models for the study of drug-induced toxicity include pluripotent stem cell-derived hepatocyte-like cells (HLCs) and complex hepatocyte-non-parenchymal cellular coculture to mimic the complex multicellular interactions that recapitulate the niche environment in the human liver. However, a specific marker of hepatocyte perturbation, required to discriminate hepatocyte damage from non-specific cellular toxicity contributed by non-hepatocyte cell types or immature differentiated cells is currently lacking, as the cytotoxicity assays routinely used in in vitro toxicology research depend on intracellular molecules which are ubiquitously present in all eukaryotic cell types. In this study, we demonstrate that microRNA-122 (miR-122) detection in cell culture media can be used as a hepatocyte-enriched in vitro marker of drug-induced toxicity in homogeneous cultures of hepatic cells, and a cell-specific marker of toxicity of hepatic cells in heterogeneous cultures such as HLCs generated from various differentiation protocols and pluripotent stem cell lines, where conventional cytotoxicity assays using generic cellular markers may not be appropriate. We show that the sensitivity of the miR-122 cytotoxicity assay is similar to conventional assays that measure lactate dehydrogenase activity and intracellular adenosine triphosphate when applied in hepatic models with high levels of intracellular miR-122, and can be multiplexed with other assays. MiR-122 as a biomarker also has the potential to bridge results in in vitro experiments to in vivo animal models and human samples using the same assay, and to link findings from clinical studies in determining the relevance of in vitro models being developed for the study of drug-induced liver injury.
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