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        TGF-β1/IL-11/MEK/ERK signaling mediates senescence-associated pulmonary fibrosis in a stress-induced premature senescence model of Bmi-1 deficiency

        Haiyun Chen,Jialong Liang,Xin Gu,Jiawen Zhou,Chunfeng Xie,Xianhui Lv,Rong Wang,Qing Liu,Zhiyuan Mao,Haijian Sun,Guoping Zuo,Dengshun Miao,Jianliang Jin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        To study whether TGF-β1/IL-11/MEK/ERK (TIME) signaling mediates senescence-associated pulmonary fibrosis (SAPF) in Bmi-1-deficient (Bmi-1−/−) mice and determines the major downstream mediator of Bmi-1 and crosstalk between p16INK4a and reactive oxygen species that regulates SAPF, phenotypes were compared among 7-week-old p16INK4a and Bmi-1 double-knockout, N-acetylcysteine (NAC)-treated Bmi-1−/−, Bmi-1−/−, and wild-type mice. Pulmonary fibroblasts and alveolar type II epithelial (AT2) cells were used for experiments. Human pulmonary tissues were tested for type Ι collagen, α-smooth muscle actin (α-SMA), p16INK4a, p53, p21, and TIME signaling by using enzyme-linked immunosorbent assay (ELISA). Our results demonstrated that Bmi-1 deficiency resulted in a shortened lifespan, ventilatory resistance, poor ventilatory compliance, and SAPF, including cell senescence, DNA damage, a senescence-associated secretory phenotype and collagen overdeposition that was mediated by the upregulation of TIME signaling. The signaling stimulated cell senescence, senescence-related secretion of TGF-β1 and IL-11 and production of collagen 1 by pulmonary fibroblasts and the epithelial-to-mesenchymal transition of AT2 cells. These processes were inhibited by anti-IL-11 or the MEK inhibitor PD98059. NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitinproteasome degradation of p16INK4a and p53. Cytoplasmic p16INK4a accumulation upregulated MEK/ERK signaling by inhibiting the translocation of pERK1/2 (Thr202/Tyr204) from the cytoplasm to the nucleus in senescent fibroblasts. The accumulation of collagen 1 and α-SMA in human lungs accompanied by cell senescence may be mediated by TIME signaling. Thus, this signaling in aging fibroblasts or AT2 cells could be a therapeutic target for preventing SAPF.

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        STRONG CONVERGENCE OF A NEW ITERATIVE ALGORITHM FOR AVERAGED MAPPINGS IN HILBERT SPACES

        Yonghong Yao,Haiyun Zhou,Rudong Chen 한국전산응용수학회 2010 Journal of applied mathematics & informatics Vol.28 No.3

        Let H be a real Hilbert space. Let T : H → H be an averaged mapping with F(T ) ≠ 0. Let {αn} be a real numbers in (0, 1). For given x0 ∈ H, let the sequence {xn} be generated iteratively by [수식]Assume that the following control conditions hold:[수식]Then {xn} converges strongly to a fixed point of T.

      • KCI등재

        STRONG CONVERGENCE OF A NEW ITERATIVE ALGORITHM FOR AVERAGED MAPPINGS IN HILBERT SPACES

        Yao, Yonghong,Zhou, Haiyun,Chen, Rudong The Korean Society for Computational and Applied M 2010 Journal of applied mathematics & informatics Vol.28 No.3

        Let H be a real Hilbert space. Let T : $H\;{\rightarrow}\;H$ be an averaged mapping with $F(T)\;{\neq}\;{\emptyset}$. Let {$\alpha_n$} be a real numbers in (0, 1). For given $x_0\;{\in}\;H$, let the sequence {$x_n$} be generated iteratively by $x_{n+1}\;=\;(1\;-\;{\alpha}_n)Tx_n$, $n\;{\geq}\;0$. Assume that the following control conditions hold: (i) $lim_{n{\rightarrow}{\infty}}\;{\alpha}_n\;=\;0$; (ii) $\sum^{\infty}_{n=0}\;{\alpha}_n\;=\;{\infty}$. Then {$x_n$} converges strongly to a fixed point of T.

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        Hydrothermal Synthesis of SnO2 Nanorod as Anode Materials for Lithium-Ion Battery

        Wei Zhang,Lili Feng,Haiyun Chen,Yinyin Zhang 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2019 NANO Vol.14 No.9

        In this study, SnO2 nanorods are successfully prepared by simple template-free hydrothermal method without surfactant. SnO intermediate with lamellar morphology is first formatted by hydrothermal method and SnO2 nanorods are obtained after calcinations. The results of XRD characterization show that lamellar structured SnO intermediate has preferred orientation in 0 0 1 direction. According to supposed mechanism during formation process of SnO2 nanorods, tiny crystal nucleus of Sn(OH)2 and a bit of SnCO3 are generated from SnCl2 and urea. Then the crystal nucleus gather together to form a nanorod. With continued reaction, nanorods gather together to form sheets and the sheets grow up to lamellar morphology and the intermediate decomposes into SnO because of the hydrothermal process. The SnO intermediate convert to SnO2 with sheets breaking to nanorods after calcination. The results of galvanostatic cell cycling show that SnO2 particle has high specific discharge capacity capacity. This experiment of SnO2 nanorod preparation provides us an effective way of easy processing, low cost, and more environmentally synthesis strategy to synthesize SnO2 nanorods.

      • KCI등재

        Detection of Rare Mutations in EGFR-ARMS-PCR-Negative Lung Adenocarcinoma by Sanger Sequencing

        Chaoyue Liang,Zhuolin Wu,Xiaohong Gan,Yuanbin Liu,You You,Chenxian Liu,Chengzhi Zhou,Ying Liang,Haiyun Mo,Allen M. Chen,Jiexia Zhang 연세대학교의과대학 2018 Yonsei medical journal Vol.59 No.1

        Purpose: This study aimed to identify potential epidermal growth factor receptor (EGFR) gene mutations in non-small cell lung cancer that went undetected by amplification refractory mutation system-Scorpion real-time PCR (ARMS-PCR). Materials and Methods: A total of 200 specimens were obtained from the First Affiliated Hospital of Guangzhou Medical University from August 2014 to August 2015. In total, 100 ARMS-negative and 100 ARMS-positive specimens were evaluated for EGFR gene mutations by Sanger sequencing. The methodology and sensitivity of each method and the outcomes of EGFR-tyrosine kinase inhibitor (TKI) therapy were analyzed. Results: Among the 100 ARMS-PCR-positive samples, 90 were positive by Sanger sequencing, while 10 cases were considered negative, because the mutation abundance was less than 10%. Among the 100 negative cases, three were positive for a rare EGFR mutation by Sanger sequencing. In the curative effect analysis of EGFR-TKIs, the progression-free survival (PFS) analysis based on ARMS and Sanger sequencing results showed no difference. However, the PFS of patients with a high abundance of EGFR mutationwas 12.4 months [95% confidence interval (CI), 11.6−12.4 months], which was significantly higher than that of patients with a low abundance of mutations detected by Sanger sequencing (95% CI, 10.7−11.3 months) (p<0.001). Conclusion: The ARMS method demonstrated higher sensitivity than Sanger sequencing, but was prone to missing mutations due to primer design. Sanger sequencing was able to detect rare EGFR mutations and deemed applicable for confirming EGFR status. A clinical trial evaluating the efficacy of EGFR-TKIs in patients with rare EGFR mutations is needed.

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