Graphene oxide assisted facile hydrothermal synthesis of LiMn_(0.6)Fe_(0.4)PO_4 nanoparticles as cathode material for lithium ion battery

Assisted by graphene oxide（GO）,nano-sized LiMn0.6Fe0.4PO4 with excellent electrochemical performance was prepared by a facile hydrothermal method as cathode material for lithium ion battery.SEM and TEM images indicate that the particle size of LiMn0.6Fe0.4PO4（S2）was about 80 nm in diameter.The discharge capacity of LiMn0.6Fe0.4PO4 nanoparticles was 140.3 mAh-g^1 in the first cycle.It showed that graphene oxide was able to restrict the growth of LiMn0.6Fe0.4PO4 and it in situ reduction of GO could improve the electrical conductivity of LiMn0.6Fe0.4PO4 material.

Neutrophil ALDH2 is a new therapeutic target for the effective treatment of sepsis-induced ARDS

Acetaldehyde dehydrogenase 2(ALDH2)mutations are commonly found in a subgroup of the Asian population.However,the role of ALDH2 in septic acute respiratory distress syndrome(ARDS)remains unknown.Here,we showed that human subjects carrying the ALDH2rs671 mutation were highly susceptible to developing septic ARDS.Intriguingly,ALDH2rs671-ARDS patients showed higher levels of blood cell-free DNA(cfDNA)and myeloperoxidase(MPO)-DNA than ALDH2WT-ARDS patients.To investigate the mechanisms underlying ALDH2 deficiency in the development of septic ARDS,we utilized Aldh2 gene knockout mice and Aldh2rs671 gene knock-in mice.In clinically relevant mouse sepsis models,Aldh2-/-mice and Aldh2rs671 mice exhibited pulmonary and circulating NETosis,a specific process that releases neutrophil extracellular traps(NETs)from neutrophils.Furthermore,we discovered that NETosis strongly promoted endothelial destruction,accelerated vascular leakage,and exacerbated septic ARDS.At the molecular level,ALDH2 increased K48-linked polyubiquitination and degradation of peptidylarginine deiminase 4(PAD4)to inhibit NETosis,which was achieved by promoting PAD4 binding to the E3 ubiquitin ligase CHIP.Pharmacological administration of the ALDH2-specific activator Alda-1 substantially alleviated septic ARDS by inhibiting NETosis.Together,our data reveal a novel ALDH2-based protective mechanism against septic ARDS,and the activation of ALDH2 may be an effective treatment strategy for sepsis.