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The dynamic characteristics of fiber-modified asphalt mixture were investigated. Cellulose fiber, polyester fiber and mineral fiber were used as additives for asphalt mixture, and the dosage was 0.3%, 0.3%, 0.4%, respectively. Dynamic modulus test using SuperPave simple performance tester (SPT) was conducted to study the dynamic modulus (E * ) and phase angle (δ) for the control asphalt mixture and fiber-modified ones at various temperatures and frequencies. Experimental results show that all fiber-modified asphalt mixtures have higher dynamic modulus compared with control mixture. The dynamic modulus master curves of each type of asphalt mixtures are determined based on nonlinear least square regression in accordance with the timetemperature superposition theory at a control temperature (21.1℃). The fatigue parameter E * ×sinδ and rutting parameter E * /sinδ of asphalt mixture are adopted to study the fatigue and rutting-resistance properties, and experimental results indicate that such properties can be improved by fiber additives.

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As a major risk factor to human health, obesity presents a massive burden to people and society. Interestingly, the obese status of parents can cause progeny’s lipid accumulation through epigenetic inheritance in multiple species. To date, many questions remain as to how lipid accumulation leads to signals that are transmitted across generations. In this study, we establish a nematode model of C. elegans raised on a high-fat diet (HFD) that leads to measurable lipid accumulation, which can transmit the lipid accumulation signal to their multigenerational progeny. Using this model, we find that transcription factors DAF-16/FOXO and SBP-1/SREBP, nuclear receptors NHR-49 and NHR-80, and delta-9 desaturases (fat-5, fat-6, and fat-7) are required for transgenerational lipid accumulation. Additionally, histone H3K4 trimethylation (H3K4me3) marks lipid metabolism genes and increases their transcription response to multigenerational obesogenic effects. In summary, this study establishes an interaction between a network of lipid metabolic genes and chromatin modifications, which work together to achieve transgenerational epigenetic inheritance of obesogenic effects.