Phosphorylation of Icariin Can Alleviate the Oxidative Stress Caused by the Duck Hepatitis Virus A through Mitogen-Activated Protein Kinases Signaling Pathways

The duck virus hepatitis (DVH) caused by the duck hepatitis virus A (DHAV) has produced extensive economic losses to the duck industry. The currently licensed commercial vaccine has shown some defects and does not completely prevent the DVH. Accordingly, a new alternative treatment for this disease is urgently needed. Previous studies have shown that icariin (ICA) and its phosphorylated derivative (pICA) possessed good anti-DHAV effects through direct and indirect antiviral pathways, such as antioxidative stress. But the antioxidant activity showed some differences between ICA and pICA. The aim of this study is to prove that ICA and pICA attenuate oxidative stress caused by DHAV in vitro and in vivo, and to investigate their mechanism of action to explain their differences in antioxidant activities. In vivo, the dynamic deaths, oxidative evaluation indexes and hepatic pathological change scores were detected. When was added the hinokitiol which showed the pro-oxidative effect as an intervention method, pICA still possessed more treatment effect than ICA. The strong correlation between mortality and oxidative stress proves that ICA and pICA alleviate oxidative stress caused by DHAV. This was also demonstrated by the addition of hydrogen peroxide (H2O2) as an intervention method in vitro. pICA can be more effective than ICA to improve duck embryonic hepatocytes (DEHs) viability and reduce the virulence of DHAV. The strong correlation between TCID50 and oxidative stress demonstrates that ICA and pICA can achieve anti-DHAV effects by inhibiting oxidative stress. In addition, the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) of ICA and pICA showed significant difference. pICA could significantly inhibit the phosphorylation of p38, extra cellular signal regulated Kinase (ERK 1/2) and c-Jun N-terminal kinase (JNK), which were related to mitogen-activated protein kinases (MAPKs) signaling pathways. Ultimately, compared to ICA, pICA exhibited more antioxidant activity that could regulate oxidative stress-related indicators, and inhibited the phosphorylation of MAPKs signaling pathway

A Time Two-Mesh Finite Difference Numerical Scheme for the Symmetric Regularized Long Wave Equation

The symmetric regularized long wave (SRLW) equation is a mathematical model used in many areas of physics; the solution of the SRLW equation can accurately describe the behavior of long waves in shallow water. To approximate the solutions of the equation, a time two-mesh (TT-M) decoupled finite difference numerical scheme is proposed in this paper to improve the efficiency of solving the SRLW equation. Based on the time two-mesh technique and two time-level finite difference method, the proposed scheme can calculate the velocity u(x,t) and density ρ(x,t) in the SRLW equation simultaneously. The linearization process involves a modification similar to the Gauss-Seidel method used for linear systems to improve the accuracy of the calculation to obtain solutions. By using the discrete energy and mathematical induction methods, the convergence results with O(τC2+τF+h2) in the discrete L∞-norm for u(x,t) and in the discrete L2-norm for ρ(x,t) are proved, respectively. The stability of the scheme was also analyzed. Finally, some numerical examples, including error estimate, computational time and preservation of conservation laws, are given to verify the efficiency of the scheme. The numerical results show that the new method preserves conservation laws of four quantities successfully. Furthermore, by comparing with the original two-level nonlinear finite difference scheme, the proposed scheme can save the CPU time

Process Parameters, Characteristics and Properties of Anodic Thermal Control Coating of Magnesium-Lithium Alloy

Effects of current density, oxidation time and sealing on thermal control properties of anodic coatings of magnesium-lithium alloy were investigated. The microstructure, thermal control properties, adhesion properties, thickness, thermal cycling test and corrosion resistance were studied. The results indicate that high infrared emittance (εH) increases with the increase of current density and oxidation time, eventually stabilizes at around 0.85. Sealing has little effect on high infrared emittance (εH); variation of εH is in the range of less than 0.05. After 96 h neutral salt spray test, the coating shows good corrosion resistance

Detecting postpartum depression in depressed people by speech features

Postpartum depression (PPD) is a depressive disorder with peripartum onset, which brings heavy burden to individuals and their families. In this paper, we propose to detect PPD in depressed people via voices. We used openSMILE for feature extraction, selected Sequential Floating Forward Selection (SFFS) algorithm for feature selection, tried different settings of features, set 5-fold cross validation and applied Support Vector Machine (SVM) on Weka for training and testing different models. The best predictive performance among our models is 69%, which suggests that the speech features could be used as a potential behavioral indicator for identifying PPD in depression. We also found that a combined impact of features and content of questions contribute to the prediction. After dimension reduction, the average value of F-measure was increased 5.2%, and the precision of PPD was rose to 75%. Comparing with demographic questions, the features of emotional induction questions have better predictive effects. &copy; Springer International Publishing AG 2018.</p

High-throughput cultivation and identification of bacteria from the plant root microbiota

Cultivating native bacteria from roots of plants grown in a given environment is essential for dissecting the functions of the root microbiota for plant growth and health with strain-specific resolution. In this study, we established a straightforward protocol for high-throughput bacterial isolation from fresh root samples using limiting dilution to ensure that most cultured bacteria originated from only one microorganism. This is followed by strain characterization using a two-sided barcode polymerase chain reaction system to identify pure and heterogeneous bacterial cultures. Our approach overcomes multiple difficulties of traditional bacterial isolation and identification methods, such as obtaining bacteria with diverse growth rates while greatly increasing throughput. To facilitate data processing, we developed an easy-to-use bioinformatic pipeline called 'Culturome' (https://github.com/YongxinLiu/Culturome) and a graphical user interface web server (http://bailab.genetics.ac.cn/culturome/). This protocol allows any research group (two or three lab members without expertise in bioinformatics) to systematically cultivate root-associated bacteria within 8-9 weeks

Encephalomyocarditis virus abrogates the interferon beta signaling pathway via its structural protein VP2

Type I interferon (IFN)-mediated antiviral responses are critical for modulating host-virus responses, and indeed, viruses have evolved strategies to antagonize this pathway. Encephalomyocarditis virus (EMCV) is an important zoonotic pathogen, which causes myocarditis, encephalitis, neurological disease, reproductive disorders, and diabetes in pigs. This study aims to understand how EMCV interacts with the IFN pathway. EMCV circumvents the type I IFN response by expressing proteins that antagonize cellular innate immunity. Here, we show that EMCV VP2 is a negative regulator of the IFN-b pathway. This occurs via the degradation of the MDA5-mediated cytoplasmic double-stranded RNA (dsRNA) antiviral sensing RIG-I-like receptor (RLR) pathway. We show that structural protein VP2 of EMCV interacts with MDA5, MAVS, and TBK1 through its C terminus. In addition, we found that EMCV VP2 could significantly degrade RLRs by the proteasomal and lysosomal pathways. For the first time, EMCV VP2 was shown to play an important role in EMCV evasion of the type I IFN signaling pathway. This study expands our understanding that EMCV utilizes its capsid protein VP2 to evade the host antiviral response. IMPORTANCE Encephalomyocarditis virus is an important pathogen that can cause encephalitis, myocarditis, neurological diseases, and reproductive disorders. It also causes huge economic losses for the swine industry worldwide. Innate immunity plays an important role in defending the host from pathogen infection. Understanding pathogen microorganisms evading the host immune system is of great importance. Currently, whether EMCV evades cytosolic RNA sensing and signaling is still poorly understood. In the present study, we found that viral protein VP2 antagonized the RLR signaling pathway by degrading MDA5, MAVS, and TBK1 protein expression to facilitate viral replication in HEK293 cells. The findings in this study identify a new mechanism for EMCV evading the host’s innate immune response, which provide new insights into the virus-host interaction and help develop new antiviral approaches against EMCV.</p

Transmembrane Protein 39A Promotes the Replication of Encephalomyocarditis Virus via Autophagy Pathway

Encephalomyocarditis virus (EMCV) causes encephalitis, myocarditis, neuropathy, reproductive disorders, and diabetes in animals. EMCV is known to induce cell autophagy; however, the molecular mechanisms underlying this remain unclear. Here, we show that the type III-transmembrane protein, transmembrane protein 39A (TMEM39A), plays a critical role in EMCV replication. We showed that EMCV GS01 strain infection upregulated TMEM39A expression. Importantly, EMCV induced autophagy in a range of host cells. The autophagy chemical inhibitor, 3-MA, inhibited EMCV replication and reduced TMEM39A expression. This is the first study demonstrating TMEM39A promoting the replication of EMCV via autophagy. Overall, we show that TMEM39A plays a positive regulatory role in EMCV proliferation and that TMEM39A expression is dependent on the autophagy pathway.</p

A high power Li-air battery enabled by a fluorocarbon additive

The mass transfer of O-2 is a critical factor to determine the rate capability of Li-air batteries (LABs). Here, with improved O-2 transport enabled by a solution-phase fluorocarbon additive 3-[2(perfluorohexyl)ethoxy]-1,2-epoxypropane, the LAB's discharge capacity was significantly elevated to 16 368 mA h g(carbon)(-1)@500 mA g(carbon)(-1) and 1792 mA h g(carbon)(-1)@5000 mA g(carbon)(-1) in N-2-O-2 (78 : 22) with power density comparable with state-of-theart Li-ion batteries

Influence of Enhanced O-2 Provision on the Discharge Performance of Li-air Batteries by Incorporating Fluoroether

As the first step during discharge, the mass transfer of oxygen should play a crucial role in Li-air batteries to tailor the growth of discharge products, however, not enough attention has been paid to this issue. Herein, we introduce an oxygen-enriching cosolvent, 1,2-(1,1,2,2-tetrafluoroethoxy) ethane (FE1), into the electrolyte, and investigate its influence on the discharge performance. The incorporation of this novel cosolvent consistently enhances the oxygen solubility of the electrolyte, and improves the oxygen diffusivity following a volcano-shape trend peaking at 50% FE1. It is interesting that the discharge capacities obtained with the investigated electrolytes share the similar volcano trends as the oxygen transport under 50mAg(carbon)(-1) and higher current densities. The improved oxygen diffusion could benefit the volumetric utilization of the air cathode, especially at the separator side, probably owing to the fast oxygen transport to moderate its concentration gradient. Our results demonstrate the importance of oxygen provision, which easily becomes the capacity-determining factor

Hypoxia-inducible factor-2α promotes tumor progression and has crosstalk with Wnt/β-catenin signaling in pancreatic cancer

Abstract Background Pancreatic cancer is a devastating disease that is characterized by persistent hypoxia. The roles of hypoxia-inducible factor-2α (hif-2α) are different to those of hif-1α, although both are critical for tumor cells to adapt to the hypoxic microenvironment. However, unlike the well-studied hif-1α, the role of hif-2α in tumors, including pancreatic cancer, is poorly understood. Methods Herein, we used a mutated hif-2α (A530T) to figure out the problem that wild-type hif-2α is quickly degraded which limits the study of its function. Using several cell lines, mouse models, and human tissues, we obtained a general picture of hif-2α in pancreatic cancer progression. Results Functional assays revealed that hif-2α promotes epithelial-to-mesenchymal transition, enhances tumor proliferation and invasion, increases stemness, facilitates angiogenesis, and up-regulates aerobic glycolysis. We identified an interaction between hif-2α and β-catenin, and found that hif-2α/β-catenin complex formation increased the activity of β-catenin and the protein stability of hif-2α. In vivo study confirmed the pro-oncogenic role of hif-2α, whose expression correlated with those of E-cadherin, vimentin, Ki-67, and CD31, but not hif-1α. A human tissue study showed that hif-2α was associated with lymph node metastasis, pathological grade, stroma abundance, vascularization and patient survival. High expression of hif-2α was also identified as an independent indicator of poor prognosis in patients with pancreatic cancer. Conclusions Our systematic study revealed the roles of hif-2α in pancreatic cancer, and may provide a novel target for this highly malignant disease