Search

The United States is the world's second‐largest producer and consumer of plastics and the largest producer of plastic waste. Understanding the sources, drivers, and destinations of plastic production, consumption, and waste is critical for the United States to develop strategies toward a zero‐plastic pollution future. Here, we characterize the dynamic material flows and stocks of plastics in the United States for nearly seven decades (1950–2018) and project the future trajectories until 2050 under various scenarios on the basis of reduce, reuse, and recycle to explore pathways toward zero plastic pollution. Our estimation shows that 1479 MMt plastics were produced in the United States from 1950 to 2018, 75 MMt waste plastics were domestically recycled, 139 MMt virgin polymers were exported, and 9 MMt recycled waste plastics were imported. Currently, about 326 MMt of plastics still remain in the society as in‐use stock, most of which (63%) are in the construction sector. Plastic pollution would almost double from 37 MMt in 2018 to 86 MMt in 2050 if current consumption pattern and waste management remain unchanged. Single strategies (i.e., plastic bag ban and extended lifespan) could only contribute limited reductions (2%–12%) of plastics pollution, and would not be able to reverse the increasing trajectory of plastic pollution until 2050. Additional measures are needed, such as improving recycling and avoiding landfilling of plastic waste. Our analysis can provide critical insights to help the United States develop long‐term strategies to mitigate and eliminate plastic pollution. [ABSTRACT FROM AUTHOR]

The industrial sector is China's major element of energy consumption and carbon emissions, and carbon emissions reduction in industrial parks has become an important foothold in carbon reduction work. Predicting the future evolution trend of carbon emissions in industrial parks under different policy orientations is of great significance for China to achieve the carbon emissions peaking and carbon neutrality goals. Based on the current status of electricity consumption and carbon emissions in industrial parks, this paper takes a light industrial park as the research object, analyzes the source of carbon emissions in this park, combines the characteristics of resource endowment and industrial structure, and considers the factors influencing society, load curve, energy supply and carbon sink, thus constructing a system dynamics model of carbon emission evolution for this park. Different influencing factors are selected to set multiple target scenarios, and the GDP, carbon emissions, carbon emissions reduction and near‐zero carbon evaluation coefficient of light industrial parks are used as characterization indicators for simulation analysis. The analysis results revealed that the comprehensive scenario set by increasing the maximum installed capacity of renewable energy units and raising the proportions of environmental and science and technology inputs while adjusting the industrial growth rate of the park performed best. In this scenario, the economic development of the park and the process of carbon emissions reduction are considered. [ABSTRACT FROM AUTHOR]

Objective: FK866 is an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which exhibits neuroprotective effects in ischemic brain injury. However, in traumatic brain injury (TBI), the role and mechanism of FK866 remain unclear. The present research was aimed to investigate whether FK866 could attenuate TBI and clarified the underlying mechanisms. Methods: A controlled cortical impact model was established, and FK866 at a dose of 5 mg/kg was administered intraperitoneally at 1 h and 6 h, then twice per day post‐TBI until sacrifice. Brain water content, Evans blue dye extravasation, modified neurological severity scores (mNSS), Morris water maze test, enzyme‐linked immunosorbent assay (ELISA), immunofluorescence staining, and western blot were performed. Results: The results demonstrated that FK866 significantly mitigated the brain edema, blood–brain barrier (BBB) disruption, and ameliorated the neurological function post‐TBI. Moreover, FK866 decreased the number of Iba‐1‐positive cells, GFAP‐positive astrocytes, and AQP4‐positive cells. FK866 reduced the protein levels of proinflammatory cytokines and inhibited NF‐κB from translocation to the nucleus. FK866 upregulated the expression of Bcl‐2, diminished the expression of Bax and caspase 3, and the number of apoptotic cells. Moreover, p38 MAPK and ERK activation were significantly inhibited by FK866. Interpretation: FK866 attenuated TBI‐induced neuroinflammation and apoptosis, at least in part, through p38/ERK MAPKs signaling pathway. [ABSTRACT FROM AUTHOR]