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| 1 | T-2 toxin induces developmental toxicity and apoptosis in zebrafish embryos显示文摘T-2 toxin is one of the most important trichothecene mycotoxins occurring in various agriculture products. The developmental toxicity of T-2 toxin and the exact mechanism of action at early life stages are not understood precisely. Zebrafish embryos were exposed to different concentrations of the toxin at 4–6 hours post fertilization(hpf) stage of development, and were observed for different developmental toxic effects at 24, 48, 72, and 144 hpf. Exposure to 0.20 μmol/L or higher concentrations of T-2 toxin significantly increased the mortality and malformation rate such as tail deformities, cardiovascular defects and behavioral changes in early developmental stages of zebrafish. T-2 toxin exposure resulted in significant increases in reactive oxygen species(ROS) production and cell apoptosis, mainly in the tail areas, as revealed by Acridine Orange staining at 24 hpf. In addition, T-2 toxin-induced severe tail deformities could be attenuated by co-exposure to reduced glutathione(GSH). T-2 toxin and GSH co-exposure induced a significant decrease of ROS production in the embryos. The overall results demonstrate that T-2 toxin is able to produce oxidative stress and induce apoptosis, which are involved in the developmental toxicity of T-2 toxin in zebrafish embryos. | Guogang Yuan Yimei Wang Xiaoyan Yuan Tingfen Zhang Jun Zhao Liuyu Huang Shuangqing Peng | 2014 | Journal of Environmental Sciences2014，26，4： | 5 |
| 2 | Influence of bicarbonate, sulfate, and electron donors on biological reduction of uranium and microbial community composition显示文摘 | Wensui Luo Wei-Min Wu Tingfen Yan Craig S. Criddle Philip M. Jardine Jizhong Zhou Baohua Gu | 2007 | Applied Microbiology and Biotechnology2007，，3： | 1 |
| 3 | Therapeutic efficacy of a tuberculosis DNA vaccine encoding heat shock protein 65 of Mycobacterium tuberculosis and the human interleukin 2 fusion gene显示文摘 | Changhong S Hai Z Limei W Jiaze A Li X Tingfen Z Zhikai X Yong Z | 2009 | Tuberculosis2009，89，1： | 1 |
| 4 | Peroxidase from proso millet exhibits endonuclease-like activity显示文摘In this study, the mechanism of DNA cleavage by cationic peroxidase from proso millet (PmPOD) was investigated. PmPOD cleaved supercoiled circular DNA into both nicked circular and linear forms via a cleavage mechanism that resembles those of native endonucleases. Inhibition and ligation studies demonstrated that reactive oxygen species and the ferriprotoporphyrin IX moiety in PmPOD are not involved in PmPOD-mediated DNA cleavage. Similar to other endonucleases, Mg ions considerably enhance the DNA cleavage activity of PmPOD. Further studies suggested that PmPOD can disrupt phosphodiester bonds in DNA and mononucleotides, indicating that it is a phosphatase. The phosphatase activity of PmPOD is higher than that of horseradish peroxidase (HRP), but the peroxidase activity of PmPOD was lower than that of HRP. PmPOD-mediated hydrolytic cleavage of DNA observed in this study is different from those reported for heme proteins. This study provides valuable insights into the distinct mechanisms underlying DNA cleavage by heme proteins. | Xiaodong Cui Tingfen Wang Wenming Wang Hongfei Wang Zhuanhua Wang | 2019 | Acta Biochimica et Biophysica Sinica2019，51，7： | 1 |
| 5 | Predictive value of T cell receptor repertoire profiling for immunosuppressive therapy in severe aplastic anemia显示文摘Increasing evidence supports the hypothesis of autologous immune attack in severe aplastic anemia(SAA):the predominant role of activated cytotoxic T cells(CTL)expressing-interferon in inhibiting the growth of bone marrow(BM)cells,putative autoantigens,and oligoclonal expansion of CD8+T cells.1 For SAA patients,the definitive therapies are immunosuppressive therapy(IST)or hematopoietic stem transplantation(HSCT). | Cunte Chen Yuling Zhang Dongpei Lu Zelong Zhang Jun Yang Xiaowei Chen Ming Zhou Wenjian Mo Caixia Wang Qinghua Cai Yumiao Li Ruiqing Zhou Shilin Xu Wei Zhou Tingfen Deng Shiyi Pan Yanli Xu Shunqing Wang Yuping Zhang | 2024 | Genes & Diseases2024，11，1： | 0 |
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