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The use of waste products in the production of asphalt binders and asphalt mixtures has become widespread due to economic and environmental benefits. In particular, the use of recycled waste plastic in asphalt binders and mixtures is gaining more attention. This review presents analyses and comparisons of various forms of waste plastic used in asphalt modification, and approaches to incorporating waste plastic into asphalt mixtures, both for single and composite modifications. It focuses on the properties of waste plastics, asphalt binders, and asphalt mixtures. Overall, the incorporation of plastic waste into asphalt mixtures can significantly improve high-temperature performance and has potential economic and environmental benefits. The performance of modified asphalt is highly dependent on multiple factors, such as waste sources, waste plastic dosages, blending conditions, and the pretreatment methods for waste plastic. There are different ways to apply waste plastics to blend into a mixture. In addition, this paper discusses the current challenges for waste plastic-modified asphalt, including the stability, low-temperature performance, modification mechanism, and laboratory problems of the blends. The use of chemical methods, such as additives and functionalization, is considered an effective way to achieve better interactions between waste plastics and the binder, as well as achieving a higher sufficiency utilization rate of waste plastics. Although both methods provide alternative options to produce waste plastic-modified asphalt with stability and high performance, the optimal proportion of materials used in the blends and the microcosmic mechanism of composite modified asphalt are not clear, and should be explored further.

Cyclin-dependent kinase 1 (CDK1) is the only necessary CDK in cell proliferation and a novel target in the development of anticancer drugs. 8-Hydroxypiperidinemethyl-baicalein (BA-j) is a novel selective CDK1 inhibitor with broad spectrum anti-cancer activity (IC50 12.3 μM) and 2 tumor xenografts. Because of the differential mechanisms controlling redox-states in normal and cancer cells, BA-j can capture oxygen free radicals (·O2−) and selectively increase the level of H2O2 in cancer cells, thereby specifically oxidize and activate the intrinsic apoptosis pathway bypassing the extrinsic death receptor pathway, thus inducing apoptosis in cancer cells rather than in normal cells. BA-j is different from cytotoxic anticancer drugs which can activate both the intrinsic apoptosis pathway and the extrinsic death receptor pathway, and therefore harm normal cells while killing cancer cells. The molecular and biochemical mechanisms of reactive oxygen species (ROS) regulation suggest that BA-j may be developed into a novel anticancer agent.