Mechanism Insights in Anticorrosion Performance of Waterborne Epoxy Coatings Reinforced by PEI-Functionalized Boron Nitride Nanosheets.

Functionalized hexagonal boron nitride nanosheets (BNNSs) have arisen as compelling anticorrosive additives, yet the precise mechanism of their corrosion resistance enhancement in coatings remains unclear. Here, polyethylenimine functionalized BNNSs (PEI-BNNSs) with approximately 6-11 layers were prepared through a "one-step" method. Then, the PEI-BNNSs/Waterborne epoxy (WEP) composite coatings were incorporated via the waterborne latex blending method for the anticorrosion of the Q235 substrate. The impedance modulus (|Z|f = 0.01 Hz) of 0.5 wt % PEI-BNNSs/WEP composite coating soaked in 3.5 wt % NaCl solution for 35 days increased by 4 orders of magnitude compared to pure WEP coating, exhibiting exceptional long-term resistance against corrosion. The positron annihilation lifetime spectroscopy and corrosion product analysis demonstrated that the reinforced anticorrosion capabilities are not solely ascribed to the "tortuous path effect" arising from BNNSs impermeability. These mechanisms also encompass the reduction in free volume fraction and radius of the free volume cavities within the composite coating brought about by the PEI molecules. Additionally, the increase in coating adhesion, promoted by PEI, plays an important role in augmenting the barrier properties against corrosive agents. This study provided a full comprehension of the role played by functionalized BNNSs in fortifying the anticorrosion attributes of WEP coatings.

Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation.

BACKGROUND: Porcine parvovirus (PPV) infection primarily causes reproductive failure of pregnant swine and results in host cell death. Boars, as an important disseminator, shed PPV to sows via semen. PPV infects and numerously replicates in boar testicle, which results in damage of swine testicle in vivo. Reactive oxygen species (ROS), a mediator of cell apoptosis, play a crucial role in the mitochondria apoptotic pathway. However, whether PPV infection induces ST cells apoptosis and ROS accumulation is still unclear. METHODS: To determine the effects of PPV infection on the apoptosis, we detected morphological changes, DNA ladder, activities of caspases, and expression of PARP in PPV-infected ST cells. Moreover, aiming to investigate the effect of PPV infection on the mitochondrial apoptotic pathway and ROS accumulation, we detected the Δψm, apoptosis-related genes, and ROS. To investigate the role of ROS in the process of PPV-induced apoptosis, the ST cells were infected with PPV and treated with the ROS antioxidants. The ROS level was measured using Reactive Oxygen Species Assay Kit and the Δψm, expression level of Bcl-2, translocation of Bax, and redistribution of mitochondria cytochrome c were tested. RESULTS: In this study, we demonstrated that PPV infection could induce apoptosis that was characterized by morphological changes, DNA fragmentation and activation of caspases. Moreover, PPV infection suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, decreased the mitochondrial transmembrane potential, and triggered the release of cytochrome c, which caused the subsequent activation of caspase-9 and caspase-3 and initiation of apoptosis. However, during the process of PPV-induced apoptosis, the protein levels of Fas and FasL were not affected. Further studies showed that PPV infection caused ROS accumulation. Inhibition of ROS could reduce mitochondrial transmembrane potential and could significantly block ST cells apoptosis via suppressing Bax translocation, cytochrome c and caspase-3 activation. CONCLUSIONS: All these results suggest that PPV-induced ROS accumulation mediates apoptosis in ST cells, which provided theoretical basis for the molecular pathogenesis of PPV infection.

Transmissible gastroenteritis virus (TGEV) infection alters the expression of cellular microRNA species that affect transcription of TGEV gene 7.

Transmissible gastroenteritis virus (TGEV) is a member of Coronaviridae family. TGEV infection has emerged as a major cause of severe gastroenteritis and leads to alterations of many cellular processes. Meanwhile, the pathogenic mechanism of TGEV is still unclear. microRNAs (miRNAs) are a novel class of small non-coding RNAs which are involved in the regulation of numerous biological processes such as viral infection and cell apoptosis. Accumulating data show that miRNAs are involved in the process of coronavirus infection such as replication of severe acute respiratory syndrome coronavirus (SARS-CoV). However, the link between miRNAs and TGEV infection is unknown. In this study, we performed microRNA microarray assay and predicted targets of altered miRNAs. The results showed TGEV infection caused the change of miRNAs profile. Then we selected miR-4331 for further analysis and subsequently identified cell division cycle-associated protein 7 (CDCA7) as the target of miR-4331. Moreover, miR-4331 showed the ability to inhibit transcription of TGEV gene 7 (a non-structure gene) via directly targeting CDCA7. In conclusion, differentially expressed miR-4331 that is caused by TGEV infection can suppress transcription of TGEV gene 7 via targeting cellular CDCA7. Our key finding is that TGEV selectively manipulates the expression of some cellular miRNAs to regulate its subgenomic transcription.