| 1. |
- Feng, Bo, et al.
(författare)
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Mechanisms of N2O Formation from Char Combustion
- 1996
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Ingår i: Energy & Fuels. - 1520-5029 .- 0887-0624. ; 10:1, s. 203-208
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Tidskriftsartikel (refereegranskat)abstract
- This paper describes an experimental study on N2O and NOx emission from char combustion. Experiments have been carried out in a fixed bed reactor in the temperature range of 973−1323 K. Oxygen concentrations for combustion, temperature, and char type have been found to have strong effects on both N2O and NOx emissions. With an increasing temperature, N2O reaches a peak at 1073 K and then decreases with temperature. At the same time NOx remains nearly the same. When oxygen concentration increases, the concentration of N2O increases and NOx first increases and then decreases. The char with higher nitrogen content emits more N2O, indicating that nitrogen oxides come from char-N. When NO is included in the inlet gases, much more N2O is produced from char combustion. This suggests that the reaction of NO + O2 + char is the main pathway for N2O formation. Another pathway, i.e., the homogeneous oxidation of HCN from the gasfication of char, seems to be important as well.
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| 2. |
- Feng, Bo, et al.
(författare)
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Nitrogen oxides emission from a circulating fluidized bed combustor
- 1998
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Ingår i: International Journal of Energy Research. - 1099-114X .- 0363-907X. ; 20:11, s. 1015-1025
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Tidskriftsartikel (refereegranskat)abstract
- Experiments were carried out in a pilot-scale circulating fluidized bed (CFB) coal combustor to investigate the mechanism of N,O formation, nitrogen oxides (including NO, and N,O) emission and the effect of temperature, excess air ratio, recirculation ratio, etc. The concentrations of nitrous oxide and nitric oxide were measured along the height of the CFB furnace. N,O concentration increased with height, and in the exit of the combustor N,O reached the highest level. NO,, however, decreased with height, showing the inverse trend compared with N,O. The N,O emission decreased sharply with the rise of temperature at the bottom of the combustor; at the same time, the NO, concentration increased.
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| 3. |
- Li, Wei, et al.
(författare)
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OxLDL-induced macrophage cytotoxicity is mediated by lysosomal rupture and modified by intralysosomal redox-active iron
- 1998
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Ingår i: Free radical research. - : Informa UK Limited. - 1071-5762 .- 1029-2470. ; 29:5, s. 389-98
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Tidskriftsartikel (refereegranskat)abstract
- Oxidized low density lipoprotein (oxLDL) is believed to play a central role in atherogenesis. LDL is oxidized in the arterial intima by mechanisms that are still only partially understood. OxLDL is then taken up by macrophages through scavenger receptor-mediated endocytosis, which then leads to cellular damage, including apoptosis. The complex mechanisms by which oxLDL induces cell injury are mostly unknown. This study has demonstrated that oxLDL-induced damage of macrophages is associated with iron-mediated intralysosomal oxidative reactions, which cause partial lysosomal rupture and ensuing apoptosis. This series of events can be prevented by pre-exposing cells to the iron-chelator, desferrioxamine (DFO), whereas it is augmented by pretreating the cells with a low molecular weight iron complex. Since both DFO and the iron complex would be taken up by endocytosis, and thus directed to the lysosomal compartment, the results suggest that the normal contents of lysosomal low molecular weight iron may play an important role in oxLDL-induced cell damage, presumably by catalyzing intralysosomal fragmentation of lipid peroxides and the formation of toxic aldehydes and oxygen-centered radicals.
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| 4. |
- Li, Wei, et al.
(författare)
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Uptake of Oxidized LDL by Macrophages Results in Partial Lysosomal Enzyme Inactivation and Relocation
- 1998
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1079-5642 .- 1524-4636. ; 18:2, s. 177-84
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Tidskriftsartikel (refereegranskat)abstract
- The cytotoxicity of oxidized LDL (oxLDL) to several types of artery wall cells might contribute to atherosclerosis by causing cell death, presumably by both apoptosis and necrosis. After its uptake into macrophage lysosomes by receptor-mediated endocytosis, oxLDL is poorly degraded, resulting in ceroid-containing foam cells. We studied the influence of oxLDL on lysosomal enzyme activity and, in particular, on lysosomal membrane stability and the modulation of these cellular characteristics by HDL and vitamin E (vit-E). Unexposed cells and cells exposed to acetylated LDL (AcLDL) were used as controls. The lysosomal marker enzymes cathepsin L and N-acetyl-β-glucosaminidase (NAβGase) were biochemically assayed in J-774 cells after fractionation. Lysosomal integrity in living cells was assayed by the acridine orange (AO) relocation test. Cathepsin D was immunocytochemically demonstrated in J-774 cells and human monocyte-derived macrophages. We found that the total activities of NAβGase and cathepsin L were significantly decreased, whereas their relative cytosolic activities were enhanced, after oxLDL exposure. Labilization of the lysosomal membranes was further proven by decreased lysosomal AO uptake and relocation to the cytosol of cathepsin D, as estimated by light and electron microscopic immunocytochemistry. HDL and vit-E diminished the cytotoxicity of oxLDL by decreasing the lysosomal damage. The results indicate that endocytosed oxLDL not only partially inactivates lysosomal enzymes but also destabilizes the acidic vacuolar compartment, causing relocation of lysosomal enzymes to the cytosol. Exposure to AcLDL resulted in its uptake with enlargement of the lysosomal apparatus, but the stability of the lysosomal membranes was not changed.
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| 5. |
- Yuan, XiMing, et al.
(författare)
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The toxicity to macrophages of oxidized low-density lipoprotein is mediated through lysosomal damage
- 1997
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Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 133:2, s. 153-61
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Tidskriftsartikel (refereegranskat)abstract
- Oxidized low-density lipoprotein (ox-LDL) has been shown to degrade poorly within the secondary lysosomes of macrophages but its possible effect on lysosomal integrity has received less attention. The effect of ultraviolet-C oxidized LDL (UVox-LDL) on cellular viability, and lysosomal membrane stability, was examined on cultured murine J-774 cells and human monocyte-derived macrophages (HMDMs). The acridine orange (AO) relocalization test was applied to study the lysosomal integrity of living cells. UVox-LDL dramatically reduced J-774 cell proliferation at a concentration of 25 microg/ml. Incubation with 5 microM copper alone, normally used to induce LDL oxidation, was also toxic. In contrast to the effects of ox-LDL, in concentrations up to 75 microg/ml, native LDL (nLDL) rather stimulated J-774 cell replication. Incubation with UVox-LDL (25-75 microg/ml) also altered cellular AO uptake, depending on time and dose: its lysosomal accumulation decreased and its cytosolic accumulation increased. This shift indicates damaged lysosomal membranes with decreased intralysosomal, and increased cytosolic, H+ concentration. Many J-774 cells exposed to UVox-LDL initially transformed into foam cells and then assumed an apoptotic-type morphology with TUNEL-positive nuclei. We conclude that ox-LDL is cytotoxic to macrophages due to oxidative damage of lysosomal membranes, with ensuing destabilization and leakage to the cytosol of lysosomal contents, such as hydrolytic enzymes, causing degeneration of apoptotic type.
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