Soo Kyung Jeong

Soo Kyung Jeong

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Soo Kyung Jeong has a total of 17 co-authors. Here are the top co-authors by number of shared publications:

  • Wol Soon Jo

    Dongnam Institute of Radiological & Medical Sciences, Busan, Republic of Korea

    2 shared publications
  • Chang Geun Lee

    Dongnam Institute of Radiological and Medical Sciences (DIRAMS), Busan, Republic of Korea

    1 shared publication
  • Chang Geun Lee

    Dongnam Institute of Radiological & Medical Sciences, Busan, Republic of Koreas

    1 shared publication
  • HyoJin Kim

    Dongnam Institute of Radiological and Medical Sciences (DIRAMS), Busan, Republic of Korea

    1 shared publication
  • Jeong-Hwa Baek

    Dongnam Institute of Radiological and Medical Sciences (DIRAMS), Busan, Republic of Korea

    1 shared publication
  • Joong Sun Kim

    College of Veterinary Medicine and BK21 Plus project team, Chonnam National University, Gwangju, Republic of Korea

    1 shared publication

Latest Publications

  • Open Access

    Automated system for establishing standard radiation dose–response curves and dose estimation for the Korean population

    by Su Jung Oh, Min Ho Jeong, Yeong-Rok Kang, Chang Geun Lee, HyoJin Kim, Yong Uk Kye, Moon-Taek Park, Jeong-Hwa Baek, Jung-Ki Kim, Joong Sun Kim, et al.

    Biological dosimetry is crucial for estimating the doses from biological samples and guiding medical interventions for accidental radiation exposure. This study aimed to derive rapid and precise dose estimates using a dicentric chromosome assay. To address the challenges of manual scoring of dicentric chromosomes, we upgraded an automatic system aimed at enhancing the precision of dicentric chromosome detection while reducing the need for human intervention. We collected blood from 30 individuals aged 20–67 years to create 30 dose-response curves aiming to investigate the differences in responses among individuals. To validate dose-estimate accuracy within a 95% confidence interval, blinded samples were categorized into three groups according to the radiation dose as follows: ≥2, ≤ 1, and 0.1 Gy. When scoring dicentric chromosomes without human review and constructing a dose–response curve, individual differences were observed. For doses ≤ 1 Gy, the standard root formula was effective; conversely, for doses ≥ 2 Gy, the regression deep neural network proved to be more ac-curate. Our developed program allowed for the rapid analysis of a large volume of dicentric chromosome images.


  • Resveratrol analogue, HS-1793, inhibits inflammatory mediator release from macrophages by interfering with the TLR4 mediated NF-κB activation

    by Wol Soon Jo, Sung Dae Kim, Soo Kyung Jeong, Su Jung Oh, Moon Taek ParK, Chang Geun Lee, Young- Rok Kang, Min Ho Jeong

    Resveratrol is known to have anti-inflammatory properties. However, high-dose resveratrol is required for optimal anti-inflammatory effects. HS-1793 is a derivative designed to be metabolically stable and more effective than resveratrol. We tested whether HS-1793 also has anti-inflammatory activity. HS-1793 effectively inhibited the mRNA and protein expression of lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in macrophages. Therefore, the production of nitric oxide (NO) and prostaglandin E2 (PGE2) was significantly attenuated. In addition, HS-1793 completely suppressed the production of inflammatory cytokines enhanced by LPS treatment along with a decrease in Toll-like receptor 4 (TLR4) expression. At the same time, the expression of myeloid differentiation factor 88 (MyD88), IL-1 receptor-associated kinase 1 (IRAK1), and TNF receptor-associated factor 6 (TRAF6) signaling molecules and the nuclear translocation of nuclear factor kappa B (NF-κB)/p65 were also downregulated. We conclusively suggest that HS-1793 also exhibits anti-inflammatory properties by effectively inhibiting TLR4-mediated NF-κB activation.