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- Karlsson, Teemu, et al.
(författare)
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Hydrogen Peroxide Ammonium Citrate Extraction: Mineral Decomposition and Preliminary Waste Rock Characterization
- 2021
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Ingår i: Minerals. - : MDPI. - 2075-163X. ; 11:7
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Tidskriftsartikel (refereegranskat)abstract
- A commonly-used method in ore exploration is hydrogen peroxide ammonium citrate (HA) extraction, which has not typically been used in waste rock characterization. In this study, the sulfide specificity and leaching of other minerals in HA extraction was evaluated and its performance was compared with the aqua regia (AR) extraction for preliminary assessment of harmful element mobility. Samples collected from several different mine sites in Finland were utilized. The waste rock sample S contents ranged from 0.3% to 5.3%, and sums of the AR extractable elements As, Cd, Co, Cu, Ni and Zn range from 120 to 8040 mg/kg. The drainage types ranged from acid high-metal to neutral low-metal, with pH’s of 3.3–7.7. Mineralogical changes that took place in the HA solution were investigated by the field emission scanning electron microscope (FE-SEM) equipped with an energy-dispersive X-ray spectroscopy analyzer (EDS) and X-ray diffraction (XRD) methods. Results of the study showed that the HA extraction appears to be a more specific method for sulfide decomposition compared with AR extraction. Sulfide minerals, especially base metal sulfides pentlandite, chalcopyrite and sphalerite, decomposed efficiently in HA extraction. However, the Fe-sulfides pyrrhotite and pyrite only decomposed incompletely. The study showed that the HA extraction results can be used in the preliminary prediction of element mobility. Based on the results, the elevated As, Cd, Co, Cu, Ni, S and Zn leachability in the HA extraction appears to predict elevated drainage concentrations. If the HA-extractable sum of As, Cd, Co, Cu, Ni and Zn is >750 mg/kg, there is an increased risk of high-metal (>1000 µg/L) drainage. Therefore, the HA extraction data, e.g., produced during ore exploration, can be utilized to preliminary screen the risks of sulfide related element mobilities from waste rock material.
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| 2. |
- Rostami, Jinar, et al.
(författare)
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Prolyl oligopeptidase inhibition by KYP-2407 increases alpha-synuclein fibril degradation in neuron-like cells
- 2020
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Ingår i: Biomedicine and Pharmacotherapy. - : Elsevier BV. - 0753-3322 .- 1950-6007. ; 131
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Tidskriftsartikel (refereegranskat)abstract
- Growing evidence emphasizes insufficient clearance of pathological alpha-synuclein (αSYN) aggregates in the progression of Parkinson's disease (PD). Consequently, cellular degradation pathways represent a potential therapeutic target. Prolyl oligopeptidase (PREP) is highly expressed in the brain and has been suggested to increase αSYN aggregation and negatively regulate the autophagy pathway. Inhibition of PREP with a small molecule inhibitor, KYP-2407, stimulates autophagy and reduces the oligomeric species of αSYN aggregates in PD mouse models. However, whether PREP inhibition has any effects on intracellular αSYN fibrils has not been studied before. In this study, the effect of KYP2407 on αSYN preformed fibrils (PFFs) was tested in SH-SY5Y cells and human astrocytes. Immunostaining analysis revealed that both cell types accumulated αSYN PFFs intracellularly but KYP-2047 decreased intracellular αSYN deposits only in SH-SY5Y cells, as astrocytes did not show any PREP activity. Western blot analysis confirmed the reduction of high molecular weight αSYN species in SH-SY5Y cell lysates, and secretion of αSYN from SH-SY5Y cells also decreased in the presence of KYP-2407. Accumulation of αSYN inside the SH-SY5Y cells resulted in an increase of the auto-lysosomal proteins p62 and LC3BII, as well as calpain 1 and 2, which have been shown to be associated with PD pathology. Notably, treatment with KYP-2407 significantly reduced p62 and LC3BII levels, indicating an increased autophagic flux, and calpain 1 and 2 levels returned to normal in the presence of KYP-2407. Our findings indicate that PREP inhibition can potentially be used as therapy to reduce the insoluble intracellular αSYN aggregates.
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