Search

Your search keyword '"Zeng, Ziyue"' showing total 164 results
Start Over Author "Zeng, Ziyue" Publication Year Range Last 10 years
164 results on '"Zeng, Ziyue"'

4. Cross-Administrative Integrated Compensation for Urban Domestic Wastewater Treatment Facilities: A Theoretic Framework and Case Study in China

Author

Zeng, Ziyue, Jiang, Lei, Wang, Dong, Wang, Ying, di Prisco, Marco, Series Editor, Chen, Sheng-Hong, Series Editor, Vayas, Ioannis, Series Editor, Kumar Shukla, Sanjay, Series Editor, Sharma, Anuj, Series Editor, Kumar, Nagesh, Series Editor, Wang, Chien Ming, Series Editor, Cui, Zhen-Dong, Series Editor, and Weng, Chih-Huang, editor

Published
2024
Full Text
View/download PDF

15. Isolation and characterisation of novel environmental bacteriophages which target the Escherichia coli LamB outer membrane protein

Author

Zeng, Ziyue and Salmond, George

Subjects
579.2, Phage, Phage-bacterium interactions, LamB protein
Abstract

Bacteriophages are viruses which infect bacteria specifically. Over the past decades, phage λ has been extensively studied, especially its interaction with the Escherichia coli LamB (EcLamB) protein receptor. Nonetheless, despite the enormous numbers and near-ubiquity of environmental phages, aside from phage λ, there is a paucity of information on other phages which target EcLamB as a receptor. In this study, to answer the question whether there are other EcLamB-targeting phages in the natural environment, a simple and convenient method was developed and used for isolating environmental phages which target a particular surface structure of a particular bacterium, in this case, the EcLamB outer membrane protein. From the enrichments with the engineered bacterial hosts, a collection of EcLamB-targeting phages (ΦZZ phages) were easily isolated. Intriguingly, unlike phage λ, an obligate EcLamB-dependent phage in the Siphoviridae family, the newly isolated ΦZZ phages alternatively recognised EcLamB or E. coli OmpC (EcOmpC) as a receptor when infecting E. coli. Furthermore, ΦZZ phages were suggested to represent new species in the Tequatrovirus genus in the Myoviridae family, based on phage morphology and genomic sequences. Most phages are thought to have a narrow host range due to their exquisite specificity in receptor-recognition. With the ability to optionally recognise two receptors, ΦZZ phages were considered relatively promiscuous. Via the heterologous expression of EcLamB on the bacterial cell surface, the host range of ΦZZ phages was further extended to three different enterobacterial genera. Besides, an interesting selection of evolved phage mutants with broader host range were isolated, and the key mutations involved in their evolution to adapt to new hosts were investigated by genomic analysis. Finally, and importantly, two ΦZZ phages were found to be putative generalised transducers, which could be exploited as tools for DNA manipulations.

Published
2020

16. Genetic dissection of the tissue‐specific roles of type III effectors and phytotoxins in the pathogenicity of Pseudomonas syringae pv. syringae to cherry

Author

Vadillo‐Dieguez, Andrea, primary, Zeng, Ziyue, additional, Mansfield, John W., additional, Grinberg, Nastasiya F., additional, Lynn, Samantha C., additional, Gregg, Adam, additional, Connell, John, additional, Harrison, Richard J., additional, Jackson, Robert W., additional, and Hulin, Michelle T., additional

Published
2024
Full Text
View/download PDF

22. Genetic dissection of the tissue-specific roles of type III effectors and phytotoxins in the pathogenicity ofPseudomonas syringaepv.syringaeto cherry

Author

Vadillo-Dieguez, Andrea, primary, Zeng, Ziyue, additional, Mansfield, John W., additional, Grinberg, Nastasiya F., additional, Lynn, Samantha C., additional, Gregg, Adam, additional, Connell, John, additional, Harrison, Richard J., additional, Jackson, Robert W., additional, and Hulin, Michelle T., additional

Published
2024
Full Text
View/download PDF

31. N-Acetylcysteine Alleviates Phenylephrine-Induced Cardiomyocyte Dysfunction via Engaging PI3K/AKT Signaling Pathway.

Author

Chao, Sheng-ping, Cheng, Wen-Lin, Yi, Wenjuan, Cai, Huan-Huan, Deng, Keqiong, Cao, Jian-Lei, Zeng, Ziyue, Wang, Hairong, and Wu, Xiaoyan

Subjects
PI3K/AKT pathway, CELLULAR signal transduction, ACETYLCYSTEINE, CELL size, PHOSPHATIDYLINOSITOL 3-kinases
Abstract

BACKGROUND Increased reactive oxygen species (ROS) and oxidative stress response lead to cardiomyocyte hypertrophy and apoptosis, which play crucial roles in the pathogenesis of heart failure. The purpose of current research was to explore the role of antioxidant N -acetylcysteine (NAC) on cardiomyocyte dysfunction and the underlying molecular mechanisms. METHODS AND RESULTS Compared with control group without NAC treatment, NAC dramatically inhibited the cell size of primary cultured neonatal rat cardiomyocytes (NRCMs) tested by immunofluorescence staining and reduced the expression of representative markers associated with hypertrophic, fibrosis and apoptosis subjected to phenylephrine administration examined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Moreover, enhanced ROS expression was attenuated, whereas activities of makers related to oxidative stress response examined by individual assay Kits, including total antioxidation capacity (T-AOC), glutathione peroxidase (GSH-Px), and primary antioxidant enzyme Superoxide dismutase (SOD) were induced by NAC treatment in NRCMs previously treated with phenylephrine. Mechanistically, we noticed that the protein expression levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) and AKT were increased by NAC stimulation. More importantly, we identified that the negative regulation of NAC in cardiomyocyte dysfunction was contributed by PI3K/AKT signaling pathway through further utilization of PI3K/AKT inhibitor (LY294002) or agonist (SC79). CONCLUSIONS Collected, NAC could attenuate cardiomyocyte dysfunction subjected to phenylephrine, partially by regulating the ROS-induced PI3K/AKT-dependent signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

45. Nek6 knockdown polarized macrophages into a pro‐inflammatory phenotype via inhibiting STAT3 expression.

Author

Wu, Xiaoyan, Deng, Ke‐Qiong, Cai, Huan‐Huan, Zeng, Ziyue, Cao, Jian‐Lei, Zhang, Lin, Lu, Zhibing, and Cheng, Wen‐Lin

Subjects
GENE expression, PERITONEAL macrophages, STAT proteins, MACROPHAGES, ATHEROSCLEROTIC plaque
Abstract

Recently macrophage polarization has emerged as playing an essential role in the oathogenesis of atherosclerosis, which is the most important underlying process in many types of cardiovascular diseases. Although Nek6 has been reported to be involved in various cellular processes, the effect of Nek6 on macrophage polarization remains unknown. Macrophages exposed to lipopolysaccharide (LPS) or IL‐4 were used to establish an in vitro model for the study of regulation of classically (M1) or alternatively (M2) activated macrophage. Bone marrow‐derived macrophages (BMDMs) transfected with short hairpin RNA‐targeting Nek6 were then in functional studies. We observed that Nek6 expression was decreased in both peritoneal macrophages (PMs) and BMDMs stimulated by LPS. This effect was seen at both mRNA and protein level. The opposite results were obtained after administration of IL‐4. Macrophage‐specific Nek6 knockdown significantly exacerbated pro‐inflammatory M1 polarized macrophage gene expression in response to LPS challenge, but the anti‐inflammatory response gene expression that is related to M2 macrophages was attenuated by Nek6 silencing followed by treatment with IL‐4. Mechanistic studies exhibited that Nek6 knockdown inhibited the phosphorylated STAT3 expression that mediated the effect on macrophage polarization regulated by AdshNek6. Moreover, decreased Nek6 expression was also observed in atherosclerotic plaques. Collectively, these evidences suggested that Nek6 acts as a crucial site in macrophage polarization, and that this operates in a STAT3‐dependent manner. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results