分块矩阵及其应用

本文利用矩阵的分块,证明了若干个关于矩阵秩的等式。     

向量空间中若干问题的入微分析和研究

对向量空间中若干有代表性的问题进行了深入细致的分析和研究.     

自校正集中式融合信息滤波器

对于带未知噪声系统和不相关噪声的多传感器随机系统,将基于相关方法得到的噪声方差带入到集中式融合最有信息滤波器,提出自校正集中式融合信息滤波器。同基于Riccatia方程的集中式融合Kalman滤波器相比,它避免了计算高维矩阵的逆,从而减少了计算负担。应用动态误差分析方法,证明了自校正集中式融合信息滤波器以概率1收敛于最优集中式融合信息滤波器,因而具有全局渐进最优性。一个带3传感器跟踪系统的实例说明其有效性。     

用循环矩阵构造整谱有向图

通过研究循环图的结构特征与其谱之间的关系,得到循环图是整谱图的条件,并由此获得了一种全新的构造整有向图的方法,可以找到了一些新的整有向图.     

线性等式约束二次规划问题的无约束的优化方法

利用矩阵理论,将线性等式约束的二次规划问题非约束化,进而给出了直接法和共轭梯度法两种优化方法。     

广义特征子空间链与若当标准形

讨论方阵A的广义特征空间与若当标准形的联系.     

SiCp／ZA-27复合材料SiC颗粒预处理工艺研究

对ＳｉＣ粒子进行子多种预处理工艺试验,得出ＳｉＣ粒了在９２０℃高温焙烧氧化,再在ＨＦ酸（１．５ｖｏｌ．）％）与丙酮混合液、丙酮中清洗球磨工艺是较优的预处理工艺。应用搅熔铸造工艺,处理后的ＳｉＣ颗粒能较易分散到含镁的ＺＡ－２７合金流中,用ＳＥＭ、ＥＤＳ、ＸＲＤ和ＴＥＭ测定和分析了预处理前后ＳｉＣ表面状态,得出ＳｉＣ颗粒表面物理,化学吸附的气体是阻止其分散进入ＺＡ－２７合金流的主要原因,ＳｉＣ表面的微     

哈密顿图的无符号拉普拉斯谱半径条件

令A(G)=(a_(ij))_(n×n)是简单图G的邻接矩阵,其中若v_i-v_j,则a_(ij)=1,否则a_(ij)=0.设D(G)是度对角矩阵,其(i,i)位置是图G的顶点v_i的度.矩阵Q(G)=D(G)+A(G)表示无符号拉普拉斯矩阵.Q(G)的最大特征根称作图G的无符号拉普拉斯谱半径,用q(G)表示.Liu,Shiu and Xue[R.Liu,W.Shui,J.Xue,Sufficient spectral conditions on Hamiltonian and traceable graphs,Linear Algebra Appl.467(2015)254-255]指出:可以通过复杂的结构分析和排除更多的例外图,当q(G)≥2n-6+4/(n-1)时,则G是哈密顿的.作为论断的有力补充,给出了图是哈密顿图的一个稍弱的充分谱条件,并给出了详细的证明和例外图.     

C*-代数上部分矩阵的投影补

在有单位元的C^＊代数上引入投影矩阵的概念,讨论了其性质,证明了C^＊代数上二阶矩阵成为投影矩阵的充分必要条件．在此基础上,研究了C^＊-代数上部分矩阵的投影补问题,得到两类二阶部分矩阵有投影补的充分必要条件．     

A functional comparison between the HER2(high)/HER3 and the HER2(low)/HER3 dimers on heregulin-β1-induced MMP-1 and MMP-9 expression in breast cancer cells

Overexpression of HER2 correlates with more aggressive tumors and increased resistance to cancer chemotherapy. However, a functional comparison between the HER2(high)/HER3 and the HER2(low)/HER3 dimers on tumor metastasis has not been conducted. Herein we examined the regulation mechanism of heregulin- β1 (HRG)-induced MMP-1 and -9 expression in breast cancer cell lines. Our results showed that the basal levels of MMP-1 and -9 mRNA and protein expression were increased by HRG treatment. In addition, HRG-induced MMP-1 and -9 expression was significantly decreased by MEK1/2 inhibitor, U0126 but not by phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294002. To confirm the role of MEK/ERK pathway on HRG-induced MMP-1 and -9 expression, MCF7 cells were transfected with constitutively active adenoviral- MEK (CA-MEK). The level of MMP-1 and -9 expressions was increased by CA-MEK. MMP-1 and -9 mRNA and protein expressions in response to HRG were higher in HER2 overexpressed cells than in vector alone. The phosphorylation of HER2, HER3, ERK, Akt, and JNK were also significantly increased in HER2 overexpressed MCF7 cells compared with vector alone. HRG-induced MMP-1 and -9 expressions were significantly decreased by lapatinib, which inhibits HER1 and HER2 activity, in both vector alone and HER2 overexpressed MCF7 cells. Finally, HRG-induced MMP-1 and MMP-9 expression was decreased by HER3 siRNA overexpression. Taken together, we suggested that HRG-induced MMP-1 and MMP-9 expression is mediated through HER3 dependent pathway and highly expressed HER2 may be associated with more aggressive metastasis than the low expressed HER2 in breast cancer cells.