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- Galkin, Maxim V., et al.
(författare)
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Hydrogen-free catalytic fractionation of woody biomass
- 2016
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Ingår i: ChemSusChem. - : Wiley. - 1864-5631 .- 1864-564X. ; 9:23, s. 3280-3287
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Tidskriftsartikel (refereegranskat)abstract
- The pulping industry could become a biorefinery if the lignin and hemicellulose components of the lignocellulose are valorized. Conversion of lignin into well-defined aromatic chemicals is still a major challenge. Lignin depolymerization reactions often occur in parallel with irreversible condensation reactions of the formed fragments. Here, we describe a strategy that markedly suppresses the undesired condensation pathways and allows to selectively transform lignin into a few aromatic compounds. Notably, applying this strategy to woody biomass at organosolv pulping conditions, the hemicellulose, cellulose, and lignin were separated and in parallel the lignin was transformed into aromatic monomers. In addition, we were able to utilize a part of the lignocellulose as an internal source of hydrogen for the reductive lignin transformations. We hope that the presented methodology will inspire researchers in the field of lignin valorization as well as pulp producers to develop more efficient biomass fractionation processes in the future.
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2. |
- Manskikh, V. N., et al.
(författare)
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Age-associated murine cardiac lesions are attenuated by the mitochondria-targeted antioxidant SkQ1
- 2015
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Ingår i: Histology and Histopathology. - 0213-3911 .- 1699-5848. ; 30:3, s. 353-360
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Tidskriftsartikel (refereegranskat)abstract
- Age-related changes in mammalian hearts often result in cardiac hypertrophy and fibrosis that are preceded by inflammatory infiltration. In this paper, we show that lifelong treatment of BALB/c and C57BL/6 mice with the mitochondria-targeted antioxidant SkQ1 retards senescence-associated myocardial disease (cardiomyopathy), cardiac hypertrophy, and diffuse myocardial fibrosis. To investigate the molecular basis of the action of SkQ1, we have applied DNA microarray analysis. The global gene expression profile in heart tissues was not significantly affected by administration of SkQ1. However, we found some small but statistically significant modifications of the pathways related to cell-to-cell contact, adhesion, and leukocyte infiltration. Probably, SkQ1-induced decrease in leukocyte and mesenchymal cell adhesion and/or infiltration lead to a reduction in age-related inflammation and subsequent fibrosis. The data indicate a causative role of mitochondrial reactive oxygen species in cardiovascular aging and imply that SkQ1 has potential as a drug against age-related cardiac dysfunction.
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