Search for: All records

High energy density lithium–sulfur batteries (LSBs) are a potential replacement for lithium-ion batteries (LIBs). However, practical lifetimes are inhibited by lithium polysulfide (LiPS) shuttling. Concurrently, plastic waste accumulation worldwide threatens our ecosystems. Herein, a fast and facile strategy to upcycle polyethylene terephthalate (PET) waste into useful materials is investigated. Dilithium terephthalate (Li2TP) and dipotassium terephthalate (K2TP) salts were synthesized from waste soda bottles via microwave depolymerization and solution coated onto glass fiber paper (GFP) separators. Salt-functionalized separators with Li2TP@GFP and K2TP@GFP mitigated LiPS shuttling and improved electrochemical performance in cells. Pore analysis and density functional theory (DFT) calculations indicate the action mechanism is synergistic physical blocking of bulky LiPS anions in nanopores and diffusion inhibition via electrostatic interactions with abundant carboxylate groups. LSBs with K2TP@GFP separator showing highest LiPS affinity and smallest pore size demonstrated enhanced initial capacity as compared to non-modified GFP by 5.4% to 648 mAh g−1, and increased cycle 100 capacity by 23% to 551 mAh g−1. Overall, K2TP@GFP retained 85% of initial capacity after 100 cycles with an average capacity fading of 0.15% per cycle. By comparison, GFP retained only 73% of initial capacity after 100 cycles with 0.27% average capacity loss, demonstrating effective LiPS retention. 

Cell death is a perpetual feature of tissue microenvironments; each day under homeostatic conditions, billions of cells die and must be swiftly cleared by phagocytes. However, cell death is not limited to this natural turnover—apoptotic cell death can be induced by infection, inflammation, or severe tissue injury. Phagocytosis of apoptotic cells is thus coupled to specific functions, from the induction of growth factors that can stimulate the replacement of dead cells to the promotion of tissue repair or tissue remodeling in the affected site. In this review, we outline the mechanisms by which phagocytes sense apoptotic cell death and discuss how phagocytosis is integrated with environmental cues to drive appropriate responses.