6 research outputs found

    Novel Architecture for Human Re-Identification with a Two-Stream Neural Network and Attention Mechanism

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    This paper proposes a novel architecture that utilises an attention mechanism in conjunction with multi-stream convolutional neural networks (CNN) to obtain high accuracy in human re-identification (Reid). The proposed architecture consists of four blocks. First, the pre-processing block prepares the input data and feeds it into a spatial-temporal two-stream CNN (STC) with two fusion points that extract the spatial-temporal features. Next, the spatial-temporal attentional LSTM block (STA) automatically fine-tunes the extracted features and assigns weight to the more critical frames in the video sequence by using an attention mechanism. Extensive experiments on four of the most popular datasets support our architecture. Finally, the results are compared with the state of the art, which shows the superiority of this approach

    GPNMB methylation: a new marker of potentially carcinogenic colon lesions

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    Abstract Background Epigenetic plays an important role in colorectal neoplasia process. There is a need to determine sound biomarkers of colorectal cancer (CRC) progression with clinical and therapeutic implications. Therefore, we aimed to examine the role and methylation status of Glyco Protein Non-Metastatic GPNM B (GPNMB) gene in normal, adenoma and CRC in African American (AA) patients. Methods The methylation status of 13 CpG sites (chr7: 23287345–23,287,426) in GPNMB gene’s promoter, was analyzed by pyrosequencing in human CRC cell lines (HCT116, SW480, and HT29) and microdissected African American paraffin embedded samples (20 normal, 21 non-advanced adenoma (NA), 48 advanced adenoma (AD), and 20 cancer tissues. GPNMB expression was analyzed by immunohistochemistry (IHC) on tissue microarrays (TMA). Correlations between GPNMB methylation and expression with clinicopathological features were analyzed. GPNMB functional analysis was performed in triplicates using cell proliferation, migration and invasion assays in HCT116 colon cell line after stable transfection with a GPNMB-cDNA expression vector. Results GPNMB methylation was lower in normal mucosa compared to CRC samples (1/20 [5%] vs. 18/20 [90%]; P  0.05) compared to the mock-transfected cells. Conclusion Our data indicate a high methylation profile leading to a lower GPNMB expression in adenoma and CRC samples. The functional analysis established GPNMB as a potential tumor suppressor gene. As such, GPNMB might be useful as a biomarker of adenomas with high carcinogenic potential

    Identification of novel mutations by exome sequencing in African American colorectal cancer patients.

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    <p>BACKGROUND: The purpose of this study was to identify genome-wide single nucleotide variants and mutations in African American patients with colorectal cancer (CRC). There is a need of such studies in African Americans, because they display a higher incidence of aggressive CRC tumors.</p> <p>METHODS: We performed whole exome sequencing (WES) on DNA from 12 normal/tumor pairs of African American CRC patient tissues. Data analysis was performed using the software package GATK (Genome Analysis Tool Kit). Normative population databases (eg, 1000 Genomes SNP database, dbSNP, and HapMap) were used for comparison. Variants were annotated using analysis of variance and were validated via Sanger sequencing.</p> <p>RESULTS: We identified somatic mutations in genes that are known targets in CRC such as APC, BRAF, KRAS, and PIK3CA. We detected novel alterations in the Wnt pathway gene, APC, within its exon 15, of which mutations are highly associated with CRC.</p> <p>CONCLUSIONS: This WES study in African American patients with CRC provides insight into the identification of novel somatic mutations in APC. Our data suggest an association between specific mutations in the Wnt signaling pathway and an increased risk of CRC. The analysis of the pathogenicity of these novel variants may shed light on the aggressive nature of CRC in African Americans. Cancer 2014. © 2014 American Cancer Society.</p
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