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An Ye,Jiqiu Qi,Yanwei Sui,Fei Yang,Fuxiang Wei,Yezeng He,Qingkun Meng,Zhi Sun 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2018 NANO Vol.13 No.7
A solid-state energy storage device has been fabricated using FeCo-selenide nanosheet arrays as positive electrode and Fe2O3 nanorod as negative electrode. As an electrode material, the ternary FeCo-selenide nanosheet arrays supported by Ni foam show a highest specific capacitance of 978 F/g (specific capacity of 163 mAh/g) at 1 A/g and a superior cycle behavior of 81.2% are obtained after 5000 cycles at current density of 4 A/g. The asymmetric supercapacitor achieves the maximum energy density of 34.6Wh/kg at the power density of 759.6 W/kg. Furthermore, the superior cycling stability with 83% retention of initial capacitance after 5000 cycles further verify the practical applications of FeCo-selenide//Fe2O3 asymmetric supercapacitor. Meanwhile, the LED bulb and the light board of "CUMT" are lighted by connecting several capacitors to form a series circuit.
Ye, Qi-Fa,Zhang, Yi-Chuan,Peng, Xiao-Qing,Long, Zhi,Ming, Ying-Zi,He, Le-Ye Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.6
Purpose: Notch is an important signaling pathway that regulates cell fate, stem cell maintenance and the initiation of differentiation in many tissues. It has been reported that activation of Notch-1 contributes to tumorigenesis. However, whether Notch signaling might have a role in chemoresistance of prostate cancer is unclear. This study aimed to investigate the effects of Notch-1 silencing on the sensitivity of prostate cancer cells to docetaxel treatment. Methods: siRNA against Notch-1 was transfected into PC-3 prostate cancer cells. Proliferation, apoptosis and cell cycle distribution were examined in the presence or absence of docetaxel by MTT and flow cytometry. Expression of $p21^{waf1/cip1}$ and Akt as well as activation of Akt in PC-3 cells were detected by Western blot and Real-time PCR. Results: Silencing of Notch-1 promoted docetaxel induced cell growth inhibition, apoptosis and cell cycle arrest in PC-3 cells. In addition, these effects were associated with increased $p21^{waf1/cip1}$ expression and decreased Akt expression and activation in PC-3 cells. Conclusion: Notch-1 promotes chemoresistance of prostate cancer and could be a potential therapeutic target.
He, Ying-Xia,Ye, Cheng-Lin,Zhang, Pei,Li, Qiao,Park, Chae Gyu,Yang, Kun,Jiang, Ling-Yu,Lv, Yin,Ying, Xiao-Ling,Ding, Hong-Hui,Huang, Hong-Ping,Mambwe Tembo, John,Li, An-Yi,Cheng, Bing,Zhang, Shu-Sheng American Society for Microbiology 2019 Infection and immunity Vol.87 No.1
<P><I>Yersinia pseudotuberculosis</I> is a Gram-negative enteropathogen and causes gastrointestinal infections. It disseminates from gut to mesenteric lymph nodes (MLNs), spleen, and liver of infected humans and animals.</P><P><I>Yersinia pseudotuberculosis</I> is a Gram-negative enteropathogen and causes gastrointestinal infections. It disseminates from gut to mesenteric lymph nodes (MLNs), spleen, and liver of infected humans and animals. Although the molecular mechanisms for dissemination and infection are unclear, many Gram-negative enteropathogens presumably invade the small intestine via Peyer’s patches to initiate dissemination. In this study, we demonstrate that <I>Y. pseudotuberculosis</I> utilizes its lipopolysaccharide (LPS) core to interact with CD209 receptors, leading to invasion of human dendritic cells (DCs) and murine macrophages. These <I>Y. pseudotuberculosis</I>-CD209 interactions result in bacterial dissemination to MLNs, spleens, and livers of both wild-type and Peyer’s patch-deficient mice. The blocking of the <I>Y. pseudotuberculosis</I>-CD209 interactions by expression of O-antigen and with oligosaccharides reduces infectivity. Based on the well-documented studies in which HIV-CD209 interaction leads to viral dissemination, we therefore propose an infection route for <I>Y. pseudotuberculosis</I> where this pathogen, after penetrating the intestinal mucosal membrane, hijacks the <I>Y. pseudotuberculosis</I>-CD209 interaction antigen-presenting cells to reach their target destinations, MLNs, spleens, and livers.</P>
Ye, Chenglin,Li, Qiao,Li, Xinyi,Park, Chae Gyu,He, Yingxia,Zhang, Yingmiao,Wu, Bicong,Xue, Ying,Yang, Kun,Lv, Yin,Ying, Xiao-Ling,Ding, Hong-Hui,Cai, Huahua,Alkraiem, Ayman Ahmad,Njiri, Olivia,Tembo, American Society for Microbiology 2019 Infection and immunity Vol.87 No.8
<P><I>Salmonella enterica</I> serovar Typhimurium, a Gram-negative bacterium, can cause infectious diseases ranging from gastroenteritis to systemic dissemination and infection. However, the molecular mechanisms underlying this bacterial dissemination have yet to be elucidated. A study indicated that using the lipopolysaccharide (LPS) core as a ligand, <I>S</I>.</P><P><I>Salmonella enterica</I> serovar Typhimurium, a Gram-negative bacterium, can cause infectious diseases ranging from gastroenteritis to systemic dissemination and infection. However, the molecular mechanisms underlying this bacterial dissemination have yet to be elucidated. A study indicated that using the lipopolysaccharide (LPS) core as a ligand, <I>S</I>. Typhimurium was able to bind human dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (hCD209a), an HIV receptor that promotes viral dissemination by hijacking antigen-presenting cells (APCs). In this study, we showed that <I>S</I>. Typhimurium interacted with CD209s, leading to the invasion of APCs and potentially the dissemination to regional lymph nodes, spleen, and liver in mice. Shielding of the exposed LPS core through the expression of O-antigen reduces dissemination and infection. Thus, we propose that similar to HIV, <I>S</I>. Typhimurium may also utilize APCs via interactions with CD209s as a way to disseminate to the lymph nodes, spleen, and liver to initiate host infection.</P>
He, Lin,Bi, Juan-Juan,Guo, Qian,Yu, Yin,Ye, Xiu-Feng Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.4
To aim of this was to observe emodin-mediated cytotoxicity and its influence on Rad51 and ERCC1 expressionin non-small cell lung cancer (NSCLC). NSCLC cells were cultured in vitro with emodin at various concentrations (0, 25, 50, 75 and $100\;{\mu}mol/L$) for 48h and the proliferation inhibition rate was determined by the MTT method. Then, NSCLC were treated with emodin (SK-MES-1 $40\;{\mu}mol/L$, A549 $70\;{\mu}mol/L$) or $20\;{\mu}mol/L$ U0126 (an ERK inhibitor) for 48 h, or with various concentrations of emodin for 48 h and the protein and mRNA expressions of ERCC1 and Rad51 were determined by RT-PCR and Western blot assay, respectively. Emodin exerted a suppressive effect on the proliferation of NSCLC in a concentration dependent manner. Protein and mRNA expression of ERCC1 and Rad51 was also significantly decreased with the dose. Vacuolar degeneration was observed in A549 and SK-MES-1 cell lines after emodin treatment by transmission electron microscopy. Emodin may thus inhibited cell proliferation in NSCLC cells by downregulation ERCC1 and Rad51.