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  • Open Access

    ARTICLE

    Energy-Efficient Scheduling Based on Task Migration Policy Using DPM for Homogeneous MPSoCs

    Hamayun Khan1,*, Irfan Ud din2, Arshad Ali3, Sami Alshmrany3

    CMC-Computers, Materials & Continua, Vol.74, No.1, pp. 965-981, 2023, DOI:10.32604/cmc.2023.031223 - 22 September 2022

    Abstract Increasing the life span and efficiency of Multiprocessor System on Chip (MPSoC) by reducing power and energy utilization has become a critical chip design challenge for multiprocessor systems. With the advancement of technology, the performance management of central processing unit (CPU) is changing. Power densities and thermal effects are quickly increasing in multi-core embedded technologies due to shrinking of chip size. When energy consumption reaches a threshold that creates a delay in complementary metal oxide semiconductor (CMOS) circuits and reduces the speed by 10%–15% because excessive on-chip temperature shortens the chip’s life cycle. In this… More >

  • Open Access

    ARTICLE

    miRNA-148b-3p targeting SOCS3 inhibits macrophage M2 polarization by JAK2/STAT3 pathway in immune thrombocytopenia

    YANG YANG, LIJUAN FU, CHUNMEI CHEN, MEIWEI HU

    BIOCELL, Vol.46, No.5, pp. 1319-1328, 2022, DOI:10.32604/biocell.2022.015760 - 06 January 2022

    Abstract Aberrant expression of miRNAs is significantly correlated with the occurrence of immune thrombocytopenic purpura (ITP). The immune imbalance of M1/M2 macrophage contributes to the development of ITP. However, the role of miR-148b-3p in macrophage phenotype imbalance remains unknown in ITP. In this study, we aimed to explore whether miR-148b-3p inhibits M2 macrophage polarization in ITP and to investigate the underlying mechanism. Peripheral blood from 22 ITP patients were collected, and real-time PCR confirmed that miR-148b-3p was up-regulated and Western blot analyses detected the expression of SOCS3 was down-regulated. Subsequent dual-luciferase reporter gene assay indicated that More >

  • Open Access

    ARTICLE

    Hardware Acceleration of Image and Video Processing on Xilinx Zynq Platform

    Praveenkumar Babu, Eswaran Parthasarathy*

    Intelligent Automation & Soft Computing, Vol.30, No.3, pp. 1063-1071, 2021, DOI:10.32604/iasc.2021.018903 - 20 August 2021

    Abstract Advancements in image and video processing are growing over the years for industrial robots, autonomous vehicles, indexing databases, surveillance, medical imaging and computer-human interaction applications. One of the major challenges in real-time image and video processing is the execution of complex functions and high computational tasks. In this paper, the hardware acceleration of different filter algorithms for both image and video processing is implemented on Xilinx Zynq®-7000 System on-Chip (SoC) device. It consists of Dual-core Cortex-A9 processors which provide computing ability to perform I/O and processing functions and software libraries using Vivado® High-Level Synthesis (HLS). In the More >

  • Open Access

    ARTICLE

    Simvastatin acts as an inhibitor of interferon gamma-induced cycloxygenase-2 expression in human THP-1 cells, but not in murine RAW264.7 cells

    CHANG SEOK LEE1, YONG JAE SHIN1, CHEOLHEE WON1, YUN-SONG LEE2, CHUNG-GYU PARK3, SANG-KYU YE1*, MYUNG-HEE CHUNG1

    BIOCELL, Vol.33, No.2, pp. 107-114, 2009, DOI:10.32604/biocell.2009.33.107

    Abstract Cyclooxygenase-2 (COX-2) is a key inflammatory response molecule, and associated with many immune functions of monocytes/macrophages. Particularly, interferon gamma (IFNγ)-induced COX-2 expression appears in inflammatory conditions such as viral infection and autoimmune diseases. Recently, statins have been reported to show variable effects on COX-2 expression, and on their cell and species type dependences. Based on the above description, we compared the effect of simvastatin on IFNγ-induced COX2 expression in human monocytes versus murine macrophages. In a result, we found that simvastatin suppresses IFNγ-induced COX-2 expression in human THP-1 monocytes, but rather, potentiates IFNγ-induced COX-2 expression More >

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