Vacancies-Induced Delocalized States Cobalt Phosphide for Binder-Free Anode Toward Stable and High-Rate Sodium-Ion Batteries.

Metal phosphides with easy synthesis, controllable morphology, and high capacity are considered as potential anodes for sodium-ion batteries (SIBs). However, the inherent shortcomings of metal phosphating materials, such as conductivity, kinetics, volume strain, etc are not satisfactory, which hinders their large-scale application. Here, a CoP@carbon nanofibers-composite containing rich Co─N─C heterointerface and phosphorus vacancies grown on carbon cloth (CoP1-x@MEC) is synthesized as SIB anode to accomplish extraordinary capacity and ultra-long cycle life. The hybrid composite nanoreactor effectively impregnates defective CoP as active reaction center while offering Co─N─C layer to buffer the volume expansion during charge-discharge process. These vast active interfaces, favored electrolyte infiltration, and a well-structured ion-electron transport network synergistically improve Na+ storage and electrode kinetics. By virtue of these superiorities, CoP1-x@MEC binder-free anode delivers superb SIBs performance including a high areal capacity (2.47 mAh cm-2@0.2 mA cm-2), high rate capability (0.443 mAh cm-2@6 mA cm-2), and long cycling stability (300 cycles without decay), thus holding great promise for inexpensive binder-free anode-based SIBs for practical applications.

BmPxt1 mediated immune response by regulating PGE2 in silkworm, Bombyx mori.

Prostaglandins (PGs) mediates the immune response of insects to multiple stimuli. Mammalian cyclooxygenase (COXs) is a key enzyme in the synthesis of PGs, and peroxinectin (Pxt) may have similar functions in some sequenced insect genomes. As a representative of Lepidoptera, the silkworm also contains PGs, but its synthetic pathway is not clear. We cloned a full-length cDNA encoding a Pxt, designated as BmPxt1, from silkworm. Sequence alignment analysis showed that the protein encoded by BmPxt1 has a conserved domain similar to Pxts, and its catalytic site is shared with the Pxt of Manduca sexta, which also produces PGs. The expression of BmPxt1 gene was the highest in the hemocytes and was induced by Nuclear Polyhedrosis Virus (NPV) challenge in the detected tissues. Moreover, we found that dsPxt1 treatment deficiency down-regulated BmPxt1 transcript levels and efficiently inhibiting hemocyte-spreading and nodule formation in silkworm. Hemocyte-spreading, nodule formation, phenoloxidase (PO) and AMP genes (attacin, defencin and moricin) were also inhibited by aspirin, a COX inhibitor. Treatment by PGE2 but not arachidonic acid (AA) rescued the immunosuppression; PGs concentrations was also inhibited by aspirin. PGE2, but not AA, treatment rescued the PGs concentrations. The COX inhibitor, aspirin, impaired the innate immune response including nodulation, encapsulation, and melanization in silkworm, while PGE2, but not arachidonic acid (AA), partially reversed these effects of aspirin. Recombinant BmsPxt1 significantly induced PO activation in larvae hemolymph, PGs concentrations and encapsulation of agarose beads. Injection of recombinant BmsPxt1 into larvae resulted in increased transcript levels of AMP genes. Our results confirmed that BmPxt1 was involved in the synthesis of PGs in the innate immune response of silkworm larvae, and provided new information for the role of BmsPxt1 secreted by silkworm in activating PO and antimicrobial peptides.