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Articles by Hua Yang
Total Records ( 7 ) for Hua Yang
  Hua Yang , Zaiyan Xu , Zhixiong Ma , Yuanzhu Xiong , Changyan Deng and Bo Zuo
  Troponin I (TnI) is a family of three muscle-specific myofibrillar proteins involved in calcium-sensitive regulation of contraction in cardiac and skeletal muscle. In this study, the full-length cDNA and genomic sequence of three genes of porcine TnI family were cloned and sequenced. The full-length cDNA of TNNI1, TNNI2, and TNNI3 genes were 989 bp, 734 bp, and 831 bp in length, which contained an open reading frame of 564, 549, and 636 nucleotides, respectively. Three Troponin I shared 54.4 ~ 58.3% similarity with each other in their predicted amino acid sequences. The TNNI1, TNNI2, and TNNI3 displayed the same genomic structure as other vertebrates and spanned over 9785 bp, 2373 bp, and 3648 bp genomic regions, respectively. The regulatory elements in the proximal promoter of TNNI2 and TNNI3 were conserved among human, mouse, and pig, but regulatory element differences existed in the TNNI1 promoter among them. Expression profiling showed that TnI genes were widely expressed in the tissues studied, with the highest expression level of TNNI1 and TNNI2 in skeletal muscle, and TNNI3 in cardiac muscle.
  Hua Yang and Feng Jiang
  Stability of stochastic systems with Markovian switching has come to play an important role in information science and engineering. The aim of the study is to discuss the stability of the semi-implicit Milstein scheme of stochastic differential delay equations with Markovian switching. The conditions of the General Mean-square (GMS) stability and Mean-square (MS) stability of the semi-implicit Milstein scheme are given by means of the conditions of the analytical solution. The obtained result shows that the numerical scheme reproduces the stability of the analytical solution to stochastic differential delay equations with Markovian switching under some conditions.
  Hua Yang , Zhou-Fang Li and Wei Wei
  WebGIS is a kind of technology, which employs the Internet as its environment, adopts Web pages as the user interface of GIS software, combines the GIS technology with the Internet and provides all kinds of GIS application with GIS function. It’s applied in all kinds of GIS field, However, In the condition of the upsurge in the number of clients, it’s easy to form "bottleneck" of computing resources in the server side, causing the server load and network latency. It can affect the user's normal use in severe condition. This study solves the bottleneck of the server-side problem by changing the architecture of the existing WebGIS. The experimental results show that the new transmission mode can solve the bottleneck problem at a certain extent.
  Hua Yang , Zhou-Fang Li and Wei Wei
  Social network play an increasingly important role in areas such as business and social activities and is causing widespread concern in academia and industry. The complexity of its properties leads the social networking phenomenon can not be model by simple mathematical theory. It has seriously hampered the development of social network data analysis techniques. The relationship of object is analyzed by using UCINET software and instance of social network. Based on information interaction between people and all kinds of information of the members of society in the social network, a social network model is built and the social network diagram is designed. This instance and analysis method is provided that is a reliable guarantee for social networking data extraction and model.
  William Kong , Hua Yang , Lili He , Jian- jun Zhao , Domenico Coppola , William S. Dalton and Jin Q. Cheng
  Transforming growth factor β (TGF-β) signaling facilitates metastasis in advanced malignancy. While a number of protein-encoding genes are known to be involved in this process, information on the role of microRNAs (miRNAs) in TGF-β-induced cell migration and invasion is still limited. By hybridizing a 515-miRNA oligonucleotide-based microarray library, a total of 28 miRNAs were found to be significantly deregulated in TGF-β-treated normal murine mammary gland (NMuMG) epithelial cells but not Smad4 knockdown NMuMG cells. Among upregulated miRNAs, miR-155 was the most significantly elevated miRNA. TGF-β induces miR-155 expression and promoter activity through Smad4. The knockdown of miR-155 suppressed TGF-β-induced epithelial-mesenchymal transition (EMT) and tight junction dissolution, as well as cell migration and invasion. Further, the ectopic expression of miR-155 reduced RhoA protein and disrupted tight junction formation. Reintroducing RhoA cDNA without the 3` untranslated region largely reversed the phenotype induced by miR-155 and TGF-β. In addition, elevated levels of miR-155 were frequently detected in invasive breast cancer tissues. These data suggest that miR-155 may play an important role in TGF-β-induced EMT and cell migration and invasion by targeting RhoA and indicate that it is a potential therapeutic target for breast cancer intervention.
  Lili He , Hua Yang , Yihong Ma , W. Jack Pledger , W. Douglas Cress and Jin Q. Cheng
  Aurora-A is a centrosome kinase and plays a pivotal role in G2/M cell cycle progression. Expression of Aurora-A is cell cycle-dependent. Levels of Aurora-A mRNA and protein are low in G1/S, accumulate during G2/M, and decrease rapidly after mitosis. Previous studies have shown regulation of the Aurora-A protein level during the cell cycle through the ubiquitin-proteasome pathway. However, the mechanism of transcriptional regulation of Aurora-A remains largely unknown. Here, we demonstrated that E2F3 modulates Aurora-A mRNA expression during the cell cycle. Ectopic expression of E2F3 induces Aurora-A expression. Stable knockdown of E2F3 decreases mRNA and protein levels of Aurora-A and delays G2/M entry. Further, E2F3 directly binds to Aurora-A promoter and stimulates the promoter activity. Deletion and mutation analyses of the Aurora-A promoter revealed that a region located 96-bp upstream of the transcription initiation site is critical for the activation of the promoter by E2F3. In addition, expression of E2F3 positively correlates with the protein level of Aurora-A in human ovarian cancer examined. These results indicate for the first time that Aurora-A is transcriptionally regulated by E2F3 during the cell cycle and that E2F3 is a causal factor for up-regulation of Aurora-A in a subset of human ovarian cancer. Thus, the E2F3-Aurora-A axis could be an important target for cancer intervention.
  Jian-Jun Zhao , Jianhong Lin , Hua Yang , William Kong , Lili He , Xu Ma , Domenico Coppola and Jin Q. Cheng
  A search for regulators of estrogen receptor α (ERα) expression has yielded a set of microRNAs (miRNAs) for which expression is specifically elevated in ERα-negative breast cancer. Here we show distinct expression of a panel of miRNAs between ERα-positive and ERα-negative breast cancer cell lines and primary tumors. Of the elevated miRNAs in ERα-negative cells, miR-221 and miR-222 directly interact with the 3`-untranslated region of ERα. Ectopic expression of miR-221 and miR-222 in MCF-7 and T47D cells resulted in a decrease in expression of ERα protein but not mRNA, whereas knockdown of miR-221 and miR-222 partially restored ERα in ERα protein-negative/mRNA-positive cells. Notably, miR-221- and/or miR-222-transfected MCF-7 and T47D cells became resistant to tamoxifen compared with vector-treated cells. Furthermore, knockdown of miR-221 and/or miR-222 sensitized MDA-MB-468 cells to tamoxifen-induced cell growth arrest and apoptosis. These findings indicate that miR-221 and miR-222 play a significant role in the regulation of ERα expression at the protein level and could be potential targets for restoring ERα expression and responding to antiestrogen therapy in a subset of breast cancers.
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