Additive operators preserving rank-additivity on symmetry matrix spaces

Xiao-Min Tang,Chong-Guang Cao 한국전산응용수학회 2004 Journal of applied mathematics & informatics Vol.14 No.-

We characterize the additive operators preserving rank-additivity on symmetry matrix spaces. Let Sn(F) be the space of all n × n symmetry matrices over a field F with 2, 3 2 F, then T is an additive injective operator preserving rank-additivity on Sn(F) if and only if there exists an invertible matrix U 2 Mn(F) and an injective field homomorphism of F to itself such that T(X) = cUXUT , 8X = (xij ) 2 Sn(F) where c 2 F,X = ((xij )). As applications, we determine the additive operators preserving minus-order on Sn(F) over the field F.

LINEAR MAPS PRESERVING PAIRS OF HERMITIAN MATRICES ON WHICH THE RANK IS ADDITIVE AND APPLICATIONS

TANG, XIAO-MIN,CAO, CHONG-GUANG 한국전산응용수학회 2005 Journal of applied mathematics & informatics Vol.19 No.1

Denote the set of n ${\times}$ n complex Hermitian matrices by Hn. A pair of n ${\times}$ n Hermitian matrices (A, B) is said to be rank-additive if rank (A+B) = rank A+rank B. We characterize the linear maps from Hn into itself that preserve the set of rank-additive pairs. As applications, the linear preservers of adjoint matrix on Hn and the Jordan homomorphisms of Hn are also given. The analogous problems on the skew Hermitian matrix space are considered.

ADDITIVE OPERATORS PRESERVING RANK-ADDITIVITY ON SYMMETRY MATRIX SPACES

Tang, Xiao-Min,Cao, Chong-Guang 한국전산응용수학회 2004 Journal of applied mathematics & informatics Vol.14 No.1

We characterize the additive operators preserving rank-additivity on symmetry matrix spaces. Let $S_{n}(F)$ be the space of all $n\;\times\;n$ symmetry matrices over a field F with 2, $3\;\in\;F^{*}$, then T is an additive injective operator preserving rank-additivity on $S_{n}(F)$ if and only if there exists an invertible matrix $U\;\in\;M_n(F)$ and an injective field homomorphism $\phi$ of F to itself such that $T(X)\;=\;cUX{\phi}U^{T},\;\forallX\;=\;(x_{ij)\;\in\;S_n(F)$ where $c\;\in;F^{*},\;X^{\phi}\;=\;(\phi(x_{ij}))$. As applications, we determine the additive operators preserving minus-order on $S_{n}(F)$ over the field F.

IRS-2 Partially Compensates for the Insulin Signal Defects in IRS-1^-/- Mice Mediated by miR-33

Tang, Chen-Yi,Man, Xiao-Fei,Guo, Yue,Tang, Hao-Neng,Tang, Jun,Zhou, Ci-La,Tan, Shu-Wen,Wang, Min,Zhou, Hou-De Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse ($Irs-1^{-/-}$) with growth retardation and subcutaneous adipocyte atrophy. $Irs-1^{-/-}$ mice exhibited mild insulin resistance, as demonstrated by the insulin tolerance test. Phosphatidylinositol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcutaneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of $Irs-1^{-/-}$ mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What's more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of $Irs-1^{-/-}$ mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

Linear maps preserving pairs of Hermitian matrices on which the rank is additive and applications

Xiao-Min Tang,Chong-Guang Cao 한국전산응용수학회 2005 Journal of applied mathematics & informatics Vol.19 No.1-2

Denote the set of n × n complex Hermitian matrices by Hn. A pair of n × n Hermitian matrices (A,B) is said to be rank-additive if rank (A+B) = rank A+rank B. We characterize the linear maps from Hn into itself that preserve the set of rank-additive pairs. As applications, the linear preservers of adjoint matrix on Hn and the Jordan homomorphisms of Hn are also given. The analogous problems on the skew Hermitian matrix space are considered.

IRS-2 Partially Compensates for the Insulin Signal Defects in IRS-1−/−Mice Mediated by miR-33

Chen-Yi Tang,Xiao-Fei Man,Yue Guo,Hao-Neng Tang,Jun Tang,Ci-La Zhou,Shu-Wen Tan,Min Wang,Hou-De Zhou 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.2

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse (Irs-1−/−) with growth retardation and subcutaneous adipocyte atrophy. Irs-1−/− mice exhibited mild insulin resistance, as demonstrat-ed by the insulin tolerance test. Phosphatidylino-sitol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcu-taneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of Irs-1−/− mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What’s more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of Irs-1−/− mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

Metastatic Axillary Lymph Node Ratio (LNR) is Prognostically Superior to pN Staging in Patients with Breast Cancer -- Results for 804 Chinese Patients from a Single Institution

Xiao, Xiang-Sheng,Tang, Hai-Lin,Xie, Xin-Hua,Li, Lai-Sheng,Kong, Ya-Nan,Wu, Min-Qing,Yang, Lu,Gao, Jie,Wei, Wei-Dong,Xie, Xiaoming Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.9

The number of axillary lymph nodes involved and retrieved are important prognostic factors in breast cancer. The purpose of our study was to investigate whether the lymph node ratio (LNR) is a better prognostic factor in predicting disease-free survival (DFS) for breast cancer patients as compared with pN staging. The analysis was based on 804 breast cancer patients who had underwent axillary lymph node dissection between 1999 and 2008 in Sun Yat-Sen University Cancer Center. Optimal cutoff points of LNR were calculated using X-tile software and validated by bootstrapping. Patients were then divided into three groups (low-, intermediate-, and high-risk) according to the cutoff points. Predicting risk factors for relapse were performed according to Cox proportional hazards analysis. DFS was estimated using the Kaplan-Meier method and compared by the log-rank test. The 5-year DFS rate decreased significantly with increasing LNRs and pN. Univariate analysis found that the pT, pN, LNR, molecule type, HER2, pTNM stage and radiotherapy well classified patients with significantly different prognosis. By multivariate analysis, only LNR classification was retained as an independent prognostic factor. Furthermore, there was a significant prognostic difference among different LNR categories for pN2 category, but no apparent prognostic difference was seen between different pN categories in any LNR category. Therefore, LNR rather than pN staging is preferable in predicting DFS in node positive breast cancer patients, and routine clinical decision-making should take the LNR into consideration.

Monosaccharide as a Central Scaffold Toward the Construction of Salicylate-Based Bidentate PTP1B Inhibitors via Click Chemistry

Tang, Yan-Hui,Hu, Min,He, Xiao-Peng,Fahnbulleh, Sando,Li, Cui,Gao, Li-Xin,Sheng, Li,Tang, Yun,Li, Jia,Chen, Guo-Rong Korean Chemical Society 2011 Bulletin of the Korean Chemical Society Vol.32 No.3

The discovery of carbohydrate-based bioactive compounds has recently received considerable interest in the drug development. This paper stresses on the application of 1-methoxy-O-glucoside as the central scaffold, whereas salicylic pharmacophores were introduced with diverse spatial orientations probing into the structural preference of an enzymatic target, i.e. protein tyrosine phosphatase 1B (PTP1B). By employing regioselective protection and deprotection strategy, 2,6-, 3,4-, 4,6- and 2,3-di-O-propynyl 1-methoxy-O-glucosides were previously synthesized and then coupled with azido salicylate via click chemistry in forming the desired bidentate salicylic glucosides with high yields. The inhibitory assay of the obtained triazolyl derivatives leads to the identification of the 2,3-disubstituted salicylic 1-methoxy-O-glucoside as the structurally privileged PTP1B inhibitor among this bidentate compound series with micromole-ranged $IC_{50}$ value and reasonable selectivity over other homologous PTPs tested. In addition, docking simulation was conducted to propose a plausible binding mode of this authorized inhibitor with PTP1B. This research might furnish new insight toward the construction of structurally different bioactive compounds based on the monosaccharide scaffold.

Over-expression of StLCYb increases b-carotene accumulation in potato tubers

Xiao-yan Song,Wen-jiao Zhu,Rui-min Tang,Jing-hui Cai,Min Chen,Qing Yang 한국식물생명공학회 2016 Plant biotechnology reports Vol.10 No.2

Lycopene b-cyclase (LCYb) is involved in the first step of the b-branch synthetic pathway of carotenoids from lycopene in plants. In this study, to explore the possibility of regulating b-carotene synthesis via the b-branchspecific pathway in potato, StLCYb gene was first isolated from potato cultivar Desiree, and its open reading frame was 1503 bp long without intron. The protein sequence of StLCYb showed high similarity with that of LCYbs in other species such as SlLCYb1, CaLCYb, NtLCYb and ApLCYb. StLCYb was expressed in all tissues and the highest level was observed in tubers followed in flowers, and the lowest level was in roots. HPLC detected an about 1.5–1.9 times increase in b-carotene content of transgenic potato tubers, in which the gene StLCYb was overexpressed, compared with the wild-type control. Besides, the expression levels of carotenoid-related genes StPSY, StPDS, StZDS, StCHYb and StZEP transcripts in the transgenic lines were significantly higher than in the wild-type control, which implied a positive regulation in promoting carotenoid synthesis. All these results suggest that b-carotene content in potato tubers could be regulated by modulating StLCYb expression.

Roles of GST-π and polβ Genes in Chemoresistance of Esophageal Carcinoma Cells

Tang, Yue,Xuan, Xiao-Yan,Li, Min,Dong, Zi-Ming Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.12

The main aim of this study was to investigate the roles of GST-${\pi}$ and $pol{\beta}$ genes in the chemoresistance of esophageal carcinoma cells. Eukaryotic expression vectors containing each gene were constructed and transfected into EC9706 cells, and the biological effects of the two genes assessed based on a resistance index. We additionally investigated the in vitro and in vivo anti-resistance effects of GST-${\pi}$ and $pol{\beta}$ genes using recombinant lentiviruses carrying siRNAs against the two genes. Our results showed that upregulation of GST-${\pi}$ and $pol{\beta}$ genes suppresses chemosensitivity of esophageal carcinoma cells to cisplatin, while downregulation of these two genes with RNAi technology reverses this chemoresistance. Multi-site injection of recombinant lentivirus targeting the GST-${\pi}$ gene into transplanted cDDP tumors effectively reversed their chemoresistant phenotype. However, the same treatment against the $pol{\beta}$ gene did not lead to significant efficacy against chemoresistance.