RESUMO
Nickel-rich LiNi0.8Co0.15Al0.015O2 (NCA) with excellent energy density is considered one of the most promising cathodes for lithium-ion batteries. Nevertheless, the stress concentration caused by Li+/Ni2+ mixing and oxygen vacancies leads to the structural collapse and obvious capacity degradation of NCA. Herein, a facile codoping of anion (F-)-cation (Mg2+) strategy is proposed to address these problems. Benefiting from the synergistic effect of F- and Mg2+, the codoped material exhibits alleviated Li+/Ni2+ mixing and demonstrates enhanced electrochemical performance at high voltage (≥4.5 V), outperformed the pristine and F-/Mg2+ single-doped counterparts. Combined experimental and theoretical studies reveal that Mg2+ and F- codoping decreases the Li+ diffusion energy barrier and enhances the Li+ transport kinetics. In particular, the codoping synergistically suppresses the Li+/Ni2+ mixing and lattice oxygen escape, and alleviates the stress-strain accumulation, thereby inhibiting crack propagation and improving the electrochemical performance of the NCA. As a consequence, the designed Li0.99Mg0.01Ni0.8Co0.15Al0.05O0.98F0.02 (Mg1+F2) demonstrates a much higher capacity retention of 82.65% than NCA (55.69%) even after 200 cycles at 2.8-4.5 V under 1 C. Furthermore, the capacity retention rate of the Mg1+F2||graphite pouch cell after 500 cycles is 89.6% compared to that of the NCA (only 79.4%).
RESUMO
Polysaccharide from Phellinus igniarius (PPI) is known for its immune-regulating effect with low toxicity. Toll like receptor 4 (TLR4) is important in both innate and adaptive immune responses and considered to be a promising target for new immune adjuvants. In this study, PPI was investigated for its effect on activating TLR4 in RAW264.7 and peritoneal macrophages. The adjuvant potential of PPI was evaluated in OVA-immunized mice. The results showed PPI treatment significantly increased the secretion and the mRNA expression of both MyD88 dependent and TRIF dependent cytokines. IRAK-1, a key molecule on the downstream of MyD88, was polyubiquitinated while IRF-3, another key molecule on the downstream of TRIF, was phosphorylated obviously after the treatment of PPI. The phosphorylation of molecules involved in both NF-κB pathway and MAPK pathway were significantly up-regulated after PPI treatment. In addition, the effects of PPI on the macrophages almost completely disappeared after treating the cells with the TLR4 antagonist TAK-242. Further in vivo results showed PPI significantly increased the serum OVA-specific antibody and the OVA-specific spleen cell proliferation. Taken together, PPI can specifically stimulate TLR4 and activate both MyD88 and TRIF pathways. PPI has immune adjuvant activity and may become a new potential immune adjuvant.