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      저자 : Hu Jingyao (검색결과 2 건)
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      • SCIESCOPUSKCI등재

        ATMOSPHERIC REFRACTION EFFECTS ON LAMOST

        SUN AIQUN,Hu JINGYAO The Korean Astronomical Society 1996 Journal of The Korean Astronomical Society Vol.29 No.suppl1

        Large field spectrographs are severely influenced by atmospheric refraction. LAMOST is a large field multi-object spectroscopy telescope with $5^{\circ}$ field of view, f/5 focus ratio and 20m focal length. There will be 4000 fibers simultaneous on it's $\phi$1.75m focal plane. Here we discuss the atmospheric refraction effects on LAMOST in two hands. One is the effect of differential refraction across the field, another is the effect of atmospheric dispersion. According to the calculation, we find that: 1. The largest deviation from center within the field is 4.;32" during a 1.5-hour integration at $80^{\circ}$ declination. 2. The directions of deviation are complex, so the deviations can't be decreased by rotating the field. We also give out the atmospheric dispersions.

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        Oncogenic E3 ubiquitin ligase NEDD4 binds to KLF8 and regulates the microRNA-132/NRF2 axis in bladder cancer

        Mao Minghuan,Yang Liang,Hu Jingyao,Liu Bing,Zhang Xiling,Liu Yili,Wang Ping,Li Hangyu 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

        The neuronally expressed developmentally downregulated 4 (NEDD4) gene encodes a ubiquitin ligase that targets the epithelial sodium channel for degradation and has been implicated in tumor growth in various cancers. Hence, in this study, we intended to characterize the functional relevance of the NEDD4-mediated Kruppel-like factor 8/microRNA-132/nuclear factor E2-related factor 2 (KLF8/miR-132/NRF2) axis in the development of bladder cancer. NEDD4 and KLF8 were overexpressed in bladder cancer tissues and were associated with poorer patient survival rates. In bladder cancer cells, NEDD4 intensified the stability and transcriptional activity of KLF8 through ubiquitination to augment cell viability and migratory ability. Our investigations revealed that NEDD4 promotes the binding of KLF8 to the miR-132 promoter region and inhibits the expression of miR-132. KLF8 inhibited the expression of miR-132 to augment the viability and migratory ability of bladder cancer cells. Furthermore, miR-132 downregulated the expression of NRF2 to restrict the viability and migratory ability of bladder cancer cells. In addition, in vivo findings verified that NEDD4 regulates the KLF8/miR-132/NRF2 axis by accelerating tumor growth and lung metastasis. In conclusion, this study highlights NEDD4 as a potential therapeutic target against tumor recurrence and metastasis in bladder cancer.

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