Zhengzhou UniversityHenan Province
Zhengzhou UniversityHenan Province
Zhai Z.,Zhengzhou UniversityHenan Province |
Jiang H.,Zhengzhou UniversityHenan Province |
Liu Y.,Zhengzhou UniversityHenan Province
Proceedings of the 2014 International Symposium on Information Technology, ISIT 2014 | Year: 2015
In order to improve the storage and transmission efficiency of CT images, this paper proposes a new adaptive truncation coding compression algorithm. First, the CT images are de-noised in wavelet domain. Second, the processed wavelet coefficients are block coded by truncating adaptively the bit stream, where the channel numbers are decided according to the relative importance of wavelet sub-bands. Finally, the reconstructed image is obtained by decoding and inverse wavelet transform. The experimental results show that the proposed algorithm can not only reduce the computational complexity, but can also improve the quality of the reconstructed image. The peak signal to noise ratio (PSNR) and the mean structural similarity (MSSIM) increase by 17% and 2%, respectively compared to the EBCOT algorithm with the same compression ratio, and the execute time reduces by 30%. © 2015 Taylor & Francis Group, London.
Jia Z.,Zhengzhou UniversityHenan province |
Yang Y.,Zhengzhou UniversityHenan province |
Dengyan Z.,Zhengzhou UniversityHenan province |
Chunyang Z.,Zhengzhou UniversityHenan province |
And 3 more authors.
Gene | Year: 2017
RAP1B is a small GTPase, which regulates multiple cellular processes. Up-regulation of RAP1B has been observed in several cancer types. Although previous study has shown that miR-518 inhibited the proliferation and invasion of esophageal squamous cell carcinoma (ESCC) cells possibly by targeting RAP1B, the expression pattern and the functions of RAP1B in ESCC are not fully understood. Here, we have fund that the expression of RAP1B was up-regulated in ESCC clinical samples. Gain-of-function and loss-of-function assays demonstrated that RAP1B promoted the growth, migration and metastasis of the ESCC cells. Moreover, the mechanism study showed that RAP1B interacted with DVL2, an important upstream regulator for beta-catenin/TCF signaling, and activated beta-catenin/TCF signaling. Taken together, our study demonstrated the oncogenic roles of RAP1B in ESCC, and suggested that RAP1B might be a therapeutic target. © 2017 Elsevier B.V.
Du J.,Anyang Normal UniversityHenan Province |
Du J.,Henan Province Key Laboratory of New Opto electronic Functional Materials |
Wang H.,Anyang Normal UniversityHenan Province |
Wang H.,Zhengzhou UniversityHenan Province |
And 15 more authors.
Electrochimica Acta | Year: 2017
Efficient production of H2 via solar-light-driven water splitting by a semiconductor-based photocatalyst without noble metals is crucial owing to increasingly severe global energy and environmental issues. However, many challenges, including the low efficiency of H2 evolution, low solar light absorption, excited electron–hole pair recombination, and slow transport of photoexcited carriers, must be resolved to enhance the H2 photoproduction efficiency and photocatalyst stability. Here, a two-step method is used to synthesize advanced H2-generating photocatalysts consisting of pyramid-like CdS nanoparticles grown on a porous TiO2 monolith, which show promising photocatalytic activity for the hydrogen evolution reaction. Furthermore, the stability of the photocatalysts is examined through long-term tests to verify their good durability. Without noble metals as cocatalysts, the photocatalyst can reach a high H2 production rate of 1048.7 μmol h−1 g−1 under UV–vis irradiation when the ratio of the CdS nanoparticles to TiO2 is 5 mol%. This unusual photocatalytic activity arises from the wide-region light adsorption due to the narrow band gap of CdS, effective separation of electrons and holes due to conduction band alignment at the CdS–TiO2 interface, and favorable reaction sites resulting from the porous structure. © 2017 Elsevier Ltd
Zhao L.,Zhengzhou UniversityHenan Province |
Zhang J.,Zhengzhou UniversityHenan Province |
Tan H.,Zhengzhou UniversityHenan Province |
Wang W.,Zhengzhou UniversityHenan Province |
And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015
Osteosa rcoma is an aggressive malignant neoplasm that exhibits osteoblastic differentiation and produces malignant osteoid. The aim of this study was to find feature genes associated with osteosarcoma and correlative gene functions which can distinguish cancer tissues from non-tumor tissues. Gene expression profile GSE14359 was downloaded from Gene Expression Omnibus (GEO) database, including 10 osteosarcoma samples and 2 normal samples. The differentially expressed genes (DEGs) between osteosarcoma and normal specimens were identified using limma package of R. DAVID was applied to mine osteosarcoma associated genes and analyze the GO enrichment on gene functions and KEGG pathways. Then, corresponding protein-protein interaction (PPI) network of DEGs was constructed based on the data collected from STRING datasets. Principal component of top10 DEGs and PPI network of top 20 DEGs were further analyzed. Finally, transcription factors were predicted by uploading the two groups of DEGs to TfactS database. A total of 437 genes, including 114 up-regulated genes and 323 down-regulated genes, were filtered as DEGs, of which 46 were associated with osteosarcoma by Disease Module. GO and KEGG pathway enrichment analysis showed that genes mainly affected the process of immune response and the development of skeletal and vascular system. The PPI network analysis elucidated that hemoglobin and histocompatibility proteins and enzymes, which were associated with immune response, were closely associated with osteosarcoma. Transcription factors MYC and SP1 were predicted to be significantly related to osteosarcoma. The discovery of gene functions and transcription factors has the potential to use in clinic for diagnosis of osteosarcoma in future. In addition, it will pave the way to studying mechanism and effective therapies for osteosarcoma. © 2015 E-Century Publishing Corporation. All rights reserved.