• Journal of Haehwa Medicine
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• v.18 no.2
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• pp.63-79
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• 2009

Atopic dermatitis induced NC/Nga mice were used to investigate the efficacy of Hyunggaeyunkyotanggamibang(HYGB) on the recovery of dermatitic symptoms through its influence on the immune related factors. The results are as below: 1. HYGB treated group showed improvement of atopic dermatitis with naked eye observation, and significant decrease of dermatitis index was observed after 14 weeks. 2. HYGB treated group showed significant decrease of the ratio of CCR3+, B220+/IgE+, and CD11b+/Gr-1+ immune cells in dorsal skin by 41.7%, 21.5%, and 23.8%, respectively. 3. HYGB treated group showed an increase of CD19+ immune cells by 10.3% in PBMC, whereas CD3+, CD3+/CD69+, NKT+ immune cells were decreased by 4.3%, 42.9%, and 21.7%, respectively. 4. HYGB treated group showed an increase in the expression of IFN-$\gamma$ in the serum by 514.3%. However, the expressions of IL-4, IL-5, IL-6, IL-13, TNF-$\alpha$, MCP-1 and RANTES were decreased by 21.2%, 69.8%, 90.5%, 28.7%, 72.2%, 26.1%, and 19.9%, respectively. Also, the expression of IgE was decreased by 44.3%. 5. HYGB treated group showed a decrease of the expression of IL-4 and IL-5 by 43% and 44.3%. The results above indicated that HYGB clinically used for atopic dermatitis treatment has objective validity, and therefore can be provided as the basic data for EBM(Evidence based medicine) construction for anti-allergic and anti-inflammatory studies.

• Proceedings of the Acoustical Society of Korea Conference
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• spring
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• pp.525-528
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• 2002

The speed of sound, transmission coefficient, and attenuation are measured around the center frequency 1 and 2 MHz in solid materials such as bone, sediment, rubber, and Lucite materials. Common and different characteristics of such materials in the sound speed, transmission coefficient, and attenuation are discussed. Ambiguities in estimating such acoustic characteristics we also addressed. Ultrasonic properties of the first and second kind waves are clarified for different materials. Discussions are concentrated on classes of sound speed, broadband ultrasonic attenuation (BUA), and correlations of sound speed and BUA with apparent density. New correlations of inverse sound speed square and BUA with apparent density are suggested.

• IMMUNE NETWORK
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• v.21 no.6
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• pp.43.1-43.14
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• 2021

Group 3 innate lymphoid cells (ILC3), which express IL-22 and IL-17A, has been introduced as one of pathologic cells in axial spondyloarthritis (axSpA). Dyslipidaemia should be managed in axSpA patients to reduce cardiovascular disease, and dyslipidaemia promotes inflammation. This study aimed to reveal the role of circulating ILC3 in axSpA and the impact of dyslipidaemia on axSpA pathogenesis. AxSpA patients with or without dyslipidaemia and healthy control were recruited. Peripheral blood samples were collected, and flow cytometry analysis of circulating ILC3 and CD4⁺ T cells was performed. The correlation between Ankylosing Spondylitis Disease Activity Score (ASDAS)-C-reactive protein (CRP) and circulating immune cells was evaluated. The effect of oxidized low-density lipoprotein cholesterol (oxLDL-C) on immune cell differentiation was confirmed. AxSpA human monocytes were cultured with with oxLDL-C, IL-22, or oxLDL-C plus IL-22 to evaluate osteoclastogenesis using tartrate-resistant acid phosphatase (TRAP) staining and real-time quantitative PCR of osteoclast-related gene expression. Total of 34 axSpA patients (13 with dyslipidaemia and 21 without) were included in the analysis. Circulating IL-22⁺ ILC3 and Th17 were significantly elevated in axSpA patients with dyslipidaemia (p=0.001 and p=0.034, respectively), and circulating IL-22⁺ ILC3 significantly correlated with ASDAS-CRP (Rho=0.4198 and p=0.0367). Stimulation with oxLDL-C significantly increased IL-22⁺ ILC3, NKp44^- ILC3, and Th17 cells, and these were reversed by CD36 blocking agent. IL-22 and oxLDL-C increased TRAP⁺ cells and osteoclast-related gene expression. This study suggested potential role of circulating IL-22⁺ ILC3 as biomarker in axSpA. Furthermore, dyslipidaemia augmented IL-22⁺ ILC3 differentiation, and oxLDL-C and IL-22 markedly increased osteoclastogenesis of axSpA.

• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.115-121
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• 2018

Upon sensing of microbial infections or endogenous danger signals in macrophages, inflammasome signaling plays a significant role in triggering inflammatory responses via producing interleukin (IL)-$1{\beta}$. Recent studies revealed that active caspase-1, a product of the inflammasome complex, causes maturation of inactive pro-IL-$1{\beta}$ into the active form. However, the underlying mechanism by which this leaderless cytokine is secreted into the extracellular space remains to be elucidated. In this study, we demonstrated that prolonged lipopolysaccharide (LPS) treatment to macrophages could trigger the unexpected maturation and extracellular release of IL-$1{\beta}$ through a nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3)-independent manner. Short-term treatment (less than 6 h) of LPS induced robust production of the IL-$1{\beta}$ precursor form inside cells but did not promote the maturation and secretion of IL-$1{\beta}$ in bone marrow-derived macrophages or peritoneal macrophages. Instead, prolonged LPS treatment (more than 12 h) led to a significant release of matured IL-$1{\beta}$ with no robust indication of caspase-1 activation. Intriguingly, this LPS-triggered secretion of IL-$1{\beta}$ was also observed in NLRP3-deficient macrophages. In addition, this unexpected IL-$1{\beta}$ release was only partially impaired by a caspase-1 and NLRP3 inflammasome inhibitor. Collectively, our results propose that prolonged exposure to LPS is able to drive the maturation and secretion of IL-$1{\beta}$ in an NLRP3 inflammasome-independent manner.

• Magazine of the Korea Concrete Institute
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• v.21 no.1
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• pp.43-47
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• 2009

• Proceedings of the KWS Conference
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• 2005.11a
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• pp.259-261
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• 2005

• Bulletin of the Korean Space Science Society
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• 1995.10a
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• pp.21-21
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• 1995

No Abstract, See Full Text

• The Bulletin of The Korean Astronomical Society
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• v.27 no.1
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• pp.21-21
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• 2002

• Bulletin of the Korean Chemical Society
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• v.21 no.5
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• pp.457-458
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• 2000

• Bulletin of the Korean Chemical Society
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• v.21 no.11
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• pp.1145-1148
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• 2000