Novel Preoxidation-Assisted Mechanism to Preciously Form and Disperse Bi2O3 Nanodots in Carbon Nanofibers for Ultralong-Life and High-Rate Sodium Storage.

Metal oxides, as promising electrode materials for sodium-ion batteries, usually need to be formed by exposure to oxygen, which usually thermally corrodes the carbon material with which they are compounded, reducing their flexibility and electrical conductivity. Herein, we present for the first time a preoxidation-assisted mechanism to prepare bismuth oxide and carbon nanofibers (Bi2O3@C-NFs) by electrospinning, using Bi2S3 nanorods as multifunctional templates. The bismuth could be oxidized by C═O bonds formed through the cyclization reaction in the high-temperature calcination process, effectively avoiding thermal corrosion of carbon in oxygen atmosphere at high temperature. More importantly, the uniformly distributed Bi2O3 nanodots and longitudinal tunnels are formed inside the S- and N-doped carbon nanofibers with the continuous diffusion of Bi generated from the decomposition of Bi2S3 nanorods and the conversion to Bi─O bonds with C═O bonds being broken. Benefiting from the structural and composition merits arising from preoxidation, Bi2O3@C-NFs self-supporting anodes show high specific capacity (439 mAh g-1 at 0.05 A g-1), superior rate performance (243 mAh g-1 at a current density of 20 A g-1), and outstanding cycling stability (211 mAh g-1 after 2000 cycles at 5 A g-1). The effective combination of the well-established electrospinning technology and the preoxidation assisted mechanism provides a new way for the preparation of metal oxide and carbon composites.

Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.

Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.

Vimentin modulates infectious porcine circovirus type 2 in PK-15 cells.

Porcine circovirus type 2 (PCV2) is the pathogen that causes postweaning multisystemic wasting syndrome, which leads to significant economic losses for swine farms worldwide. However, the infection mechanism of PCV2 is not completely understood yet. Vimentin is a part of the cytoskeleton network and plays an important role in several virus infections. It is not clear whether vimentin has a role in PCV2 infection nor how it affects PCV2 infection. In this study, the function of vimentin in PK-15 cells infected with PCV2 has been elucidated. We found that vimentin had a restrictive effect on the replication of PCV2 in PK-15 cells. Overexpression of vimentin by transferred pCAGGS-vimentin and down-regulation by the respective scrambled small interfering RNA showed that vimentin restricted the replication and virion production of PCV2. A special interaction between vimentin and PCV2 Cap protein was observed using laser confocal microscopy and immunoprecipitation assay. Moreover, overexpression of vimentin could decrease NF-κB activity and increase PCV2-induced caspase-3 activity in PK-15 cells. These data suggest that vimentin is involved in the replication of PCV2 and has a restrictive effect on it, which is helpful in the study of the replication mechanism of PCV2.