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  • Open Access

    ARTICLE

    Integration of Digital Twins and Artificial Intelligence for Classifying Cardiac Ischemia

    Mohamed Ammar1,*, Hamed Al-Raweshidy2,*

    Journal on Artificial Intelligence, Vol.5, pp. 195-218, 2023, DOI:10.32604/jai.2023.045199 - 29 December 2023

    Abstract Despite advances in intelligent medical care, difficulties remain. Due to its complicated governance, designing, planning, improving, and managing the cardiac system remains difficult. Oversight, including intelligent monitoring, feedback systems, and management practises, is unsuccessful. Current platforms cannot deliver lifelong personal health management services. Insufficient accuracy in patient crisis warning programmes. No frequent, direct interaction between healthcare workers and patients is visible. Physical medical systems and intelligent information systems are not integrated. This study introduces the Advanced Cardiac Twin (ACT) model integrated with Artificial Neural Network (ANN) to handle real-time monitoring, decision-making, and crisis prediction. THINGSPEAK… More >

  • Open Access

    ARTICLE

    APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis

    ZHAOHUI HU1,2, XIANGJUN DING3, YUYAO JI2, XIAOHONG LIU4,*, ZHIWEN DING2,*

    BIOCELL, Vol.45, No.3, pp. 745-749, 2021, DOI:10.32604/biocell.2021.013293 - 03 March 2021

    Abstract Apurine/pyrimidine-free endonuclease 1 (APEX1) is a multifunctional enzyme that contributes to oxidizationmediated DNA-cleaved base excision repair and redox activation of transcription factors. However, the role of APEX1 during cardiomyocyte oxidative stress injury is not completely understood. In the present study, whether APEX1 protects oxidative damage-induced cardiomyocytes was investigated. mRNA and protein expression levels of APEX1 were downregulated in the mouse model of cardiac ischemia-reperfusion injury. Furthermore, the expression of APEX1 in hydrogen peroxide (H2O2)-treated neonatal mice cardiomyocytes was also decreased. APEX1 knockdown aggravated H2O2-treated cardiomyocyte apoptosis indexes. By contrast, APEX1 overexpression reversed H2O2-induced oxidative damage, as demonstrated More >

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