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Compaction of hot mix asphalt (HMA) requires high temperatures in the range of 125 to 145 ° C to ensure the fluidity of asphalt binder and, therefore, the workability of asphalt mixtures. The high temperatures are associated with high energy consumption, and higher NOx emissions, and can also accelerate the aging of asphalt binders. In previous research, the authors have developed two approaches for improving the compactability of asphalt mixtures: (1) addition of Graphite Nanoplatelets (GNPs), and (2) optimizing aggregate packing. This research explores the effects of these two approaches, and the combination of them, on reducing compaction temperatures while the production temperature is kept at the traditional levels. A reduction in compaction temperatures is desired for prolonging the paving window, extending the hauling distance, reducing the energy consumption for reheating, and for reducing the number of repairs and their negative environmental and safety effects, by improving the durability of the mixtures. A Superpave asphalt mixture was chosen as the control mixture. Three modified mixtures were designed, respectively, by (1) adding 6% GNP by the weight of binder, (2) optimizing aggregate packing, and (3) combining the two previous approaches. Gyratory compaction tests were performed on the four mixtures at two compaction temperatures: 135 ° C (the compaction temperature of the control mixture) and 95 ° C. A method was proposed based on the gyratory compaction to estimate the compaction temperature of the mixtures. The results show that all the three methods increase the compactability of mixtures and thus significantly reduce the compaction temperatures. Method 3 (combining GNP modification and aggregate packing optimization) has the most significant effect, followed by method 1 (GNP modification), and method 2 (aggregate packing optimization). [ABSTRACT FROM AUTHOR]

Digital manufacturing has transformed many industries but has had only a limited impact in the construction sector. To capitalize on advanced manufacturing techniques, this paper introduces a radically new connection approach for gravity structural steel frames. The proposed intermeshed steel connection (ISC) exploits robotic abilities to cut structural steel member ends precisely to accelerate deployment and offer better disassembly options over existing approaches. Forces are transferred through common bearing surfaces at multiple contact points, and connections can be secured by small locking pieces. This paper introduces the geometry, manufacturing, and initial analysis and test results of the connection. The paper demonstrates the ability of the connection to (1) be manufactured within current industrial tolerances, (2) be erected and disassembled, and (3) perform at expected design levels. [ABSTRACT FROM AUTHOR]

DJ-1 was recently reported to be involved in the cardioprotection of hypoxic preconditioning (HPC) against hypoxia/reoxygenation (H/R)-induced oxidative stress damage, by preserving mitochondrial complex I activity and, subsequently, inhibiting mitochondrial reactive oxygen species (ROS) generation. However, the molecular mechanism by which HPC enables mitochondrial translocation of DJ-1, which has no mitochondria-targeting sequence, to preserve mitochondrial complex I, is largely unknown. In this study, co-immunoprecipitation data showed that DJ-1 was associated with glucose-regulated protein 75 (Grp75), and this association was significantly enhanced after HPC. Immunofluorescence imaging and Western blot analysis showed that HPC substantially enhanced the translocation of DJ-1 from cytosol to mitochondria in H9c2 cells subjected to H/R, which was mimicked by DJ-1 overexpression induced by pFlag-DJ-1 transfection. Importantly, knockdown of Grp75 markedly reduced the mitochondrial translocation of DJ-1 induced by HPC and pFlag-DJ-1 transfection. Moreover, HPC promoted the association of DJ-1 with mitochondrial complex I subunits ND1 and NDUFA4, improved complex I activity, and inhibited mitochondria-derived ROS production and subsequent oxidative stress damage after H/R, which was also mimicked by pFlag-DJ-1 transfection. Intriguingly, these effects of HPC and pFlag-DJ-1 transfection were also prevented by Grp75 knockdown. In conclusion, these results indicated that HPC promotes the translocation of DJ-1 from cytosol to mitochondria in a Grp75-dependent manner and Grp75 is required for DJ-1-mediated protection of HPC on H/R-induced mitochondrial complex I defect and subsequent oxidative stress damage. [ABSTRACT FROM AUTHOR]

DJ-1 was recently reported to be involved in the cardioprotection of hypoxic preconditioning (HPC) against hypoxia/reoxygenation (H/R)-induced oxidative stress damage, by preserving mitochondrial complex I activity and, subsequently, inhibiting mitochondrial reactive oxygen species (ROS) generation. However, the molecular mechanism by which HPC enables mitochondrial translocation of DJ-1, which has no mitochondria-targeting sequence, to preserve mitochondrial complex I, is largely unknown. In this study, co-immunoprecipitation data showed that DJ-1 was associated with glucose-regulated protein 75 (Grp75), and this association was significantly enhanced after HPC. Immunofluorescence imaging and Western blot analysis showed that HPC substantially enhanced the translocation of DJ-1 from cytosol to mitochondria in H9c2 cells subjected to H/R, which was mimicked by DJ-1 overexpression induced by pFlag-DJ-1 transfection. Importantly, knockdown of Grp75 markedly reduced the mitochondrial translocation of DJ-1 induced by HPC and pFlag-DJ-1 transfection. Moreover, HPC promoted the association of DJ-1 with mitochondrial complex I subunits ND1 and NDUFA4, improved complex I activity, and inhibited mitochondria-derived ROS production and subsequent oxidative stress damage after H/R, which was also mimicked by pFlag-DJ-1 transfection. Intriguingly, these effects of HPC and pFlag-DJ-1 transfection were also prevented by Grp75 knockdown. In conclusion, these results indicated that HPC promotes the translocation of DJ-1 from cytosol to mitochondria in a Grp75-dependent manner and Grp75 is required for DJ-1-mediated protection of HPC on H/R-induced mitochondrial complex I defect and subsequent oxidative stress damage.