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- 저자 : Bao-Sheng Qiu (검색결과 4 건)
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IDEMPOTENCE PRESERVING MAPS ON SPACES OF TRIANGULAR MATRICES
Sheng, Yu-Qiu,Zheng, Bao-Dong,Zhang, Xian 한국전산응용수학회 2007 Journal of applied mathematics & informatics Vol.25 No.1
Suppose F is an arbitrary field. Let ${\mid}F{\mid}$ be the number of the elements of F. Let $T_{n}(F)$ be the space of all $n{\times}n$ upper-triangular matrices over F. A map ${\Psi}\;:\;T_{n}(F)\;{\rightarrow}\;T_{n}(F)$ is said to preserve idempotence if $A-{\lambda}B$ is idempotent if and only if ${\Psi}(A)-{\lambda}{\Psi}(B)$ is idempotent for any $A,\;B\;{\in}\;T_{n}(F)$ and ${\lambda}\;{\in}\;F$. It is shown that: when the characteristic of F is not 2, ${\mid}F{\mid}\;>\;3$ and $n\;{\geq}\;3,\;{\Psi}\;:\;T_{n}(F)\;{\rightarrow}\;T_{n}(F)$ is a map preserving idempotence if and only if there exists an invertible matrix $P\;{\in}\;T_{n}(F)$ such that either ${\Phi}(A)\;=\;PAP^{-1}$ for every $A\;{\in}\;T_{n}(F)\;or\;{\Psi}(A)=PJA^{t}JP^{-1}$ for every $P\;{\in}\;T_{n}(F)$, where $J\;=\;{\sum}^{n}_{i-1}\;E_{i,n+1-i}\;and\;E_{ij}$ is the matrix with 1 in the (i,j)th entry and 0 elsewhere.
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Induction of Apoptosis by IGFBP3 Overexpression in Hepatocellular Carcinoma Cells
Han, Jian-Jun,Xue, De-Wen,Han, Qiu-Rong,Liang, Xiao-Hong,Xie, Li,Li, Sheng,Wu, Hui-Yong,Song, Bao Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23
Background: The insulin-like growth factor (IGF) system comprises a group of proteins that play key roles in regulating cell growth, differentiation, and apoptosis in a variety of cellular systems. The aim of this study was to investigate the role of insulin-like growth factor binding protein 3 (IGFBP3) in hepatocellular carcinoma. Materials and Methods: Expression of IGF2, IGFBP3, and PTEN was analyzed by qRT-PCR. Lentivirus vectors were used to overexpress IGFBP3 in hepatocellular carcinoma cell (HCC) lines. The effect of IGFBP3 on proliferation was investigated by MTT and colony formation assays. Results: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells. Conclusions: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells.
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Zhang, Gui-Fang,Zhou, Min,Bao, Xie-Bing,Qiu, Hui-Ying,Li, Zheng,Xue, Sheng-Li Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.9
Purpose: To compare the relative merits of imatinib and allogeneic hematopoietic stem cell transplantation (allo-HSCT) for chronic myelogenous leukemia (CML). Materials and Methods: This cohort study was designed to compare the outcomes of imatinib (n=292) versus allo-HSCT (n=141) for CML, the clinical data of these patients being retrospectively analyzed so as to compare the event free survival (EFS) and overall survival (OS) between these two groups with patients in the chronic phase (CP) and advanced phases, including accelerate (AP) and blast phases (BP). Results: (1) Patients treated with imatinib (278 in the CP) demonstrated superior EFS, OS, 5-year EFS and 5-year OS rates of 88.5% versus 70.0% (P<0.05), 93.2% versus 80.0% (P<0.05), 84% versus 75.0% (P<0.05) and 92% versus 79.0% (P<0.05), respectively, to those treated with allo-HSCT (120 patients in the CP). (2) Both treatments resulted in similar survival, with EFS and OS rates of 42.9% versus 47.6% (P>0.05), 42.9% versus 57.1% (P> 0.05), respectively, for imatinib (14 patients in the AP and BP) and allo-HSCT (21 patients in the AP and BP). Conclusions: Imatinib confers significant survival advantage (EFS and OS) for CML patients with CP compared with allo-HSCT treatment. However, the outcomes are equally good with both treatments in AP and BP patients.
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Xiang Gao,Wen-Li Ai,Huan Gong,Li-Juan Cui,Bo-Xia Chen,Hong-Yi Luo,Zhong-Chun Zhang,Bao-Sheng Qiu 한국식물생명공학회 2016 Plant biotechnology reports Vol.10 No.2
Transgenic research was preformed by transferring a cyanobacterial (Nostoc flagelliforme) iron superoxide dismutase gene (NfFeSOD) into heavy metal hyperaccumulator Sedum alfredii via Agrobacterium-mediated method. Beyond expectation, NfFeSOD-overexpressing S. alfredii plants exhibited profound impairments, including plant growth retardation, abnormal root architecture, and reduced leaf greenness, photosynthetic efficiency and metal accumulation efficiency. Although transgenic plants appeared physiologically sensitive to high temperature, a higher relative biomass growth was still observed under long-term high temperature and osmotic stresses. Further investigation found that reactive oxygen species (ROS) homeostasis of transgenic plants was significantly affected, being ~50 % reduction of H2O2 level relative to wild-type plants. Gene transcription including ROS responsive genes was overall attenuated in transgenic plants, being more significant at normal temperature than at high temperature. In addition, ascorbate peroxidase (APX) activity was increased nearly twofolds in transgenic plants as compared to wild-type control. It may be inferred that ectopic NfFeSOD overexpression gives rise to a substantial increase of APX activity and leads to a sharp reduction of H2O2 level, thus impairing basal ROS signaling and plant growth. Specific genetic background of S. alfredii may be responsible for this sharp reduction of H2O2 level induced by NfFeSOD overexpression. S. alfredii plant has acclimated to elevated levels of ROS induced by heavy metals in native habitats and should require high ROS levels for basal signaling. We thus suppose that a sustained disturbance of high basal ROS signaling in metal hyperaccumulators may instead incur very sensitive response and thus result in profound growth impairments.
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