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Background: The purpose of this study was to investigate the potential involvement of pyruvate kinase M2 (PKM2), an enzyme acting as a rate-limiting enzyme in the final phase of glycolysis, in the regulation of glial activation and brain damage of intracerebral hemorrhage (ICH). Methods: Western blotting and immunofluorescence were performed to investigate PKM2 expression, terminal deoxynucleotidyl transferase deoxyurinary triphosphate (dUTP) nick end labeling staining, hematoxylin and eosin staining, and behavioral tests were employed to evaluate the brain damage of ICH mice, and RNA-seq and bioinformatic analyses were performed to detect gene expression changes in ICH mice treated with TEPP-46. Results: Increased PKM2 levels in perihematomal brain tissue were found starting from 3 days following ICH and peaked at 5 and 7 days post ICH. The increased expression of PKM2 was mainly co-localized with glial fibrillary acidic protein (GFAP)+ astrocytes and ionized calcium binding adaptor molecule-1 (IBA-1)+ microglia. Furthermore, we observed a notable increase in the nuclear translocation of PKM2 in glial cells following ICH. TEPP-46 treatment significantly reduced PKM2 nuclear translocation, and effectively attenuated glial activation and brain injury, and improved functional recovery of mice with ICH. RNA-seq data indicated that 91.1% (205/225) of differentially expressed genes (DEGs) were down-regulated in the TEPP-46 treated groups compared with the vehicle-treated groups in ICH brains. Furthermore, bioinformatic analyses revealed that these down-regulated DEGs were involved in a variety of biological processes, including autophagy and metabolic processes. In addition, the majority of these downregulated DEGs had a primary high expression in neurons, with subsequent expression seen in endothelial cells, microglia, and astrocytes. Conclusions: These results indicate that increased PKM2 nuclear translocation promotes the activation of glial cells after ICH, hence aggravating ICH-induced brain damage, and aggravates the brain injury induced by ICH. This highlights a potential therapeutic target for inhibiting glial activation to attenuate brain injury after ICH. [ABSTRACT FROM AUTHOR]

The energy dissipation capacities and fragments distribution of concrete exposed to high temperature under impact loading are studied. Dynamic compressive tests of concrete at room temperature and after exposure to elevated temperatures ranging from 200 to 800 °C are conducted by using a split Hopkinson pressure bar with 100 mm in diameter. The effects of high temperature and impact velocity on dissipated energy,failure mode and fractal dimension of fragments are analyzed. The results indicate that the dissipated energy grows with the increase in impact velocity and strain rate at the same temperature; and at fixed impact velocity,the dissipated energy decreases with the increase in the exposure temperature. The fragment-size distribution of concrete fragments statistically has fractal property subjected to impact loading. An increase in temperature and impact velocity results in a greater crushing degree and a larger fractal dimension value. There is a positive correlation between dissipated energy and fractal dimension at the same temperature. As a result,the impact crushing of concrete at various temperatures and impact velocities is a fractal evolution process driven by external energy. [ABSTRACT FROM AUTHOR]