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- 저자 : Deng Haixia (검색결과 4 건)
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Deng, Haixia,Belharouak, Ilias,Sun, Yang-Kook,Amine, Khalil Royal Society of Chemistry 2009 Journal of materials chemistry Vol.19 No.26
<P>Manganese-rich and cobalt-free compounds of Li<SUB><I>x</I></SUB>Ni<SUB>0.25</SUB>Mn<SUB>0.75</SUB>O<SUB><I>y</I></SUB> (0.5 ≤ <I>x</I> ≤ 2, 2 ≤ <I>y</I> ≤ 2.75) were investigated as the positive electrode materials for high energy lithium-ion batteries. Compounds with <I>x</I> = 0.5, 1, 1.25, 1.5, and 2 were prepared by a solid-state reaction from the same carbonate precursor, Ni<SUB>0.25</SUB>Mn<SUB>0.75</SUB>CO<SUB>3</SUB>, with an appropriate amount of Li<SUB>2</SUB>CO<SUB>3</SUB>. The structural and physical characteristics of these phases were determined by X-ray diffraction and scanning electron microscopy. With an increase of the lithium content, the Li<SUB><I>x</I></SUB>Ni<SUB>0.25</SUB>Mn<SUB>0.75</SUB>O<SUB><I>y</I></SUB> evolved from a spinel (Fd3&cmb.macr;m) structure (<I>x</I> = 0.5) to a mixed spinel-layered (Fd3&cmb.macr;m and C2/c) structure (<I>x</I> = 1 and 1.25), to a more layered (R3&cmb.macr;m and C2/c) structure (<I>x</I> = 1.5 and 2). A similar structural trend was found for samples prepared from NiMn<SUB>2</SUB>O<SUB>4</SUB>–Mn<SUB>2</SUB>O<SUB>3</SUB> mixed oxide, itself prepared by thermal decomposition of Ni<SUB>0.25</SUB>Mn<SUB>0.75</SUB>CO<SUB>3</SUB> carbonate precursor, to which appropriate amounts of Li<SUB>2</SUB>CO<SUB>3</SUB> were added. An increase of the lithium content also affected the size of the primary particles and the roughness of the secondary particles, without any substantial change of their spherical morphology and packing densities. Further results showed that the electrochemical performance and safety characteristics of the Li<SUB><I>x</I></SUB>Ni<SUB>0.25</SUB>Mn<SUB>0.75</SUB>O<SUB><I>y</I></SUB> materials were primarily governed by their structures.</P> <P>Graphic Abstract</P><P>Despite the integration of different phases within each particle, these nickel and manganese oxide precursors served to prepare lithiated materials for high-power and high-energy density lithium-ion batteries. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=b904098f'> </P>
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Pan, Haixia,Yang, Linhan,Bai, Hansong,Luo, Jing,Deng, Ying The Korean Society of Ginseng 2022 Journal of Ginseng Research Vol.46 No.5
Background: Ginsenoside Rg3 and gemcitabine have mutual enhancing antitumor effects. However, the underlying mechanisms are not clear. This study explored the influence of ginsenoside Rg3 on Zinc finger protein 91 homolog (ZFP91) expression in pancreatic adenocarcinoma (PAAD) and their regulatory mechanisms on gemcitabine sensitivity. Methods: RNA-seq and survival data from The Cancer Genome Atlas (TCGA)-PAAD and Genotype-Tissue Expression (GTEx) were used for in-silicon analysis. PANC-1, BxPC-3, and PANC-1 gemcitabine-resistant (PANC-1/GR) cells were used for in vitro analysis. PANC-1 derived tumor xenograft nude mice model was used to assess the influence of ginsenoside Rg3 and ZFP91 on tumor growth in vivo. Results: Ginsenoside Rg3 reduced ZFP91 expression in PAAD cells in a dose-dependent manner. ZFP91 upregulation was associated with significantly shorter survival of patients with PAAD. ZFP91 overexpression induced gemcitabine resistance, which was partly conquered by ginsenoside Rg3 treatment. ZFP91 depletion sensitized PANC-1/GR cells to gemcitabine treatment. ZFP91 interacted with Testis-Specific Y-Encoded-Like Protein 2 (TSPYL2), induced its poly-ubiquitination, and promoted proteasomal degradation. Ginsenoside Rg3 treatment weakened ZFP91-induced TSPYL2 poly-ubiquitination and degradation. Enforced TSPYL2 expression increased gemcitabine sensitivity of PAAD cells and partly reversed induced gemcitabine resistance in PANC-1/GR cells. Conclusion: Ginsenoside Rg3 can increase gemcitabine sensitivity of pancreatic adenocarcinoma at least via reducing ZFP91 mediated TSPYL2 destabilization.
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LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway
Tao Zhang,Yu Ge,Daijun Wang,Qin Liu,Shuchen Sun,Lingyang Hua,Jiaojiao Deng,Shihai Luan,Haixia Cheng,Qing Xie,Ye Gong,Tao Zhang 한국분자세포생물학회 2022 Molecules and cells Vol.45 No.6
Malignant meningiomas often show invasive growth that makes complete tumor resection challenging, and they are more prone to recur after radical resection. Invasive meningioma associated transcript 1 (IMAT1) is a long noncoding RNA located on Homo sapiens chromosome 17 that was identified by our team based on absolute expression differences in invasive and non-invasive meningiomas. Our studies indicated that IMAT1 was highly expressed in invasive meningiomas compared with non-invasive meningiomas. In vitro studies showed that IMAT1 promoted meningioma cell invasion through the inactivation of the Krüppel-like factor 4 (KLF4)/hsa-miR22-3p/Snai1 pathway by acting as a sponge for hsa-miR22-3p, and IMAT1 knockdown effectively restored the tumor suppressive properties of KLF4 by preserving its tumor suppressor pathway. In vivo experiments confirmed that IMAT1 silencing could significantly inhibit the growth of subcutaneous tumors and prolong the survival period of tumor-bearing mice. Our findings demonstrated that the high expression of IMAT1 is the inherent reason for the loss of the tumor suppressive properties of KLF4 during meningioma progression. Therefore, we believe that IMAT1 may be a potential biological marker and treatment target for meningiomas.
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