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Articles by Ying He
Total Records ( 6 ) for Ying He
  Ying He , Fei Zhong , Wangbin Cao and Manfu Zhang
  Canine parvovirus type 2 (CPV-2) has emerged as a pathogen of new acute infectious disease in dogs. It affects primarily young animals where it can cause haemorrhagic enteritis and myocarditis. Receptor binding is a key step in the life cycles of all animal viruses. It has been reported that the specific binding to transferrin receptor (TfR) on cell membranes plays an important role in tissue tropism and host ranges of CPV-2. In this study, the entry and the subcellular localization of viral particles and TfR in the cells of FK81 and MDCK were analyzed; the distribution of TfR and infectious ability of CPV-2 were determined in the cells of various primary tissue cultures from dog fetus. We observed complicated temporal patterns of CPV-2 virus particle trafficking during post-incubation with cells of FK81 and MDCK. The virus particles were located in the cytoplasm 4-8 h after inoculation, they appeared in nuclei at 12-16 h of post-incubation, then reappeared in cytoplasm at 24 h again; they distributed all over the cellular organelles after 32 h incubation. The virus and the transferrin were co-located in the perinuclear cytoplasm after 2 h of incubation with the FK81 cells; addition of excessive transferrin decreased the rate of infection of CPV-2, but did not block virus entry. We found that CPV-2 replicated in primary culture cells of the liver, kidney, cardiac muscle, spleen and intestinal epithelia but not of the lung and internalization of transferrin receptor in primary cells was related to the culture tropism of CPV-2. These results confirmed that the TfR is critical for CPV-2 infection with both cell lines and primary tissue cells from fetes.
  Ping Zhao , Ying He , Yuefeng Chu , Baoyu Li , Pengcheng Gao , Xuan Zhang , Haiyan Zhao , Youjun Shang and Zhongxin Lu
  Mycoplasma capricolum sub sp. capripneumoniae (Mccp) is the causative agent of contagious capripleuropneumonia (CCPP) in goats. To develop more effective vaccines against CCPP, three protein sequences were optimized, in terms of codon usage bias, GC content, restriction enzymes, CIS-acting elements and repeat sequences, which are critical for efficient gene expression. These three proteins, respectively are the pyruvate dehydrogenase E1 component alpha subunit (PDHA), pyruvate dehydrogenase complex E1 component beta subunit (PDHB) and dihydrolipoylysine-residue acetyltransferase components of the pyruvate dehydrogenase complex (PDHC). The three optimized genes were expressed in E. coli and the relevant proteins were analyzed further by in vivo expression detection and antibody detection. The results showed the following: (1) A significantly higher level of serum antibodies against the three proteins were detected with convalescent sera and immunized sera, which demonstrated that the three proteins were expressed in vivo. (2) Goats antisera tests against the three proteins showed that they could all elicit humoral immunity with potential antigenicity and reactogenicity. (3) The results suggested that these three proteins (PDHA, PDHB and PDHC) have strong potential as vaccine candidates.
  Hong-Jiang Gao , Hong Sun , Bang-Hai Xu , Ying He and Zheng Qin
  The aim of this study is to demonstrate the approach of stepwise development of a distributed transaction mechanism for information retrieval systems. In this study, we formally develop an abstract model of transactions in Event-B for an IR system, in which fault tolerance is provided in the distributed transaction execution. We starts from an abstract system specification and gradually introduce implementation details in a series of correctness-preserving transformations, where complex system properties (such as fault tolerant) could be specified in a structured and rigorous way. During each transformation, the refinement between the abstract specification of the system and its detailed design is verified. Using Event-B, we achieve a high degree of automatic proof via this incremental approach.
  Qilin Cheng , Ying He , Vladimir Pavlinek , Chunzhong Li and Petr Saha
  In this work, we demonstrate a simple route to the preparation of bulk quantities of polypyrrole/titanate (PPy/TN) composite nanofibers using cetyl trimethylammonium bromide (CTAB) as a structure-directing agent. Titanate (TN) nanowires and CTAB act as a template for fabrication of the composite nanofibers. The structural characterization shows that the resulting nanocomposite exhibits core-shell nanofiber networks and the average diameter of the nanofibers is around 50–90 nm. The electrical conductivity measurements reveal that the addition of TN nanowires slightly enhances the conductivity of the composite. The ac conductivity follows the power law, which varies with the mass ratio of pyrrole monomer to TN. A possible mechanism is also proposed to interpret the formation of the PPy/TN composite nanofiber networks.
  Zailian Lu , Wei Liu , Huizhe Huang , Ying He , Ying Han , Yanning Rui , Yanhai Wang , Qinxi Li , Ka Ruan , Zhiyun Ye , Boon Chuan Low , Anming Meng and Sheng-Cai Lin
  Axin plays an architectural role in many important signaling pathways that control various aspects of development and tumorigenesis, including the Wnt, transforming growth factor-β, MAP kinase pathways, as well as p53 activation cascades. It is encoded by the mouse Fused (Fu) locus; the AxinFu allele is caused by insertion of an IAP transposon. AxinFu/Fu mice display varying phenotypes ranging from embryonic lethality to relatively normal adulthood with kinky tails. However, the protein product(s) has not been identified or characterized. In the present study, we conducted immunoprecipitation using brain extracts from the AxinFu mice with specific antibodies against different regions of Axin and found that a truncated Axin containing amino acids 1–596 (designated as AxinFu-NT) and the full-length complement of Axin (AxinWT) can both be generated from the AxinFu allele. When tested for functionality changes, AxinFu-NT was found to abolish Axin-mediated activation of JNK, which plays a critical role in dorsoventral patterning. Together with a proteomics approach, we found that AxinFu-NT contains a previously uncharacterized dimerization domain and can form a heterodimeric interaction with AxinWT. The AxinFu-NT/AxinWT is not conducive to JNK activation, providing a molecular explanation for the dominant negative effect of AxinFu-NT on JNK activation by wild-type Axin. Importantly, AxinFu-NT exhibits no difference in the inhibition of Wnt signaling compared with AxinWT as determined by reporter gene assays, interaction with key Wnt regulators, and expression of Wnt marker genes in zebrafish embryos, suggesting that altered JNK signaling contributes, at least in part, to the developmental defects seen in AxinFu mice.
  Weiwen Deng , Mude Shi , Meifang Han , Jin Zhong , Zhenhu Li , Weina Li , Yu Hu , Lingchen Yan , Jie Wang , Ying He , Hong Tang , Vincent Deubel , Xiaoping Luo , Qin Ning and Bing Sun
  Induction of Type I IFNs is a central event in antiviral responses and must be tightly controlled. The protein kinase TBK1 is critically involved in virus-triggered type I IFN signaling. In this study, we identify an alternatively spliced isoform of TBK1, termed TBK1s, which lacks exons 3–6. Upon Sendai virus (SeV) infection, TBK1s is induced in both human and mouse cells and binds to RIG-1, disrupting the interaction between RIG-I and VISA. Consistent with that result, overexpression of TBK1s inhibits IRF3 nuclear translocation and leads to a shutdown of SeV-triggered IFN-β production. Taken together, our data indicate that TBK1s plays an inhibitory role in virus-triggered IFN-β signaling pathways.
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