Kosin Medical Journal

Young-Ho Kim

2 Articles

Clinical efficacy and safety of autologous serum intramuscular injection in patients with mild-to-moderate atopic dermatitis: a prospective, open-label, uncontrolled study: Gil-Soon Choi, Jong Bin Park, Young-Ho Kim, Hee-Kyoo Kim; Kosin Med J. 2024;39(1):51-59. Published online March 19, 2024; DOI: https://doi.org/10.7180/kmj.24.101

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Background
Autologous blood therapy (ABT) has been used to treat atopic dermatitis (AD) for over a century, even though evidence supporting its efficacy is lacking. We aimed to investigate the effectiveness and safety of autologous serum intramuscular injection (ASIM), which is a modified form of ABT, in treating mild-to-moderate AD.
Methods
This study was a 12-week, open-label, prospective, uncontrolled trial. Following a 4-week run-in period, 22 out of 25 screened patients received ASIM once a week for 4 weeks in conjunction with standard treatment. The primary outcome measure was the Eczema Area and Severity Index (EASI), while the secondary outcomes included the Scoring Atopic Dermatitis (SCORAD) score, Dermatologic Life Quality Index (DLQI), and patient ratings of pruritus, sleep difficulty, disease status, and treatment effectiveness. Safety parameters were also assessed.
Results
EASI scores showed a non-statistically significant trend toward improvement during ASIM intervention. Patients with at least a 50% improvement in the EASI score at 4 weeks were older and had lower peripheral eosinophil counts (p<0.05). Secondary endpoints, including the SCORAD score, pruritus, sleep difficulty, and DLQI, demonstrated statistically significant improvements at week 4 compared to baseline (p<0.05). No significant adverse reactions were observed.
Conclusions
This pioneering study suggests that repeated ASIM may improve the clinical symptoms of mild-to-moderate AD, particularly in terms of pruritus and overall quality of life. However, further research with a larger sample size is required to establish the clinical significance of these findings.

Citations

Citations to this article as recorded by

What are the clinical usefulness and scientific value of intramuscular injection of autologous serum (autologous serum therapy) in patients with atopic dermatitis?
Dong-Ho Nahm
Kosin Medical Journal.2024; 39(1): 1. CrossRef

Quercetin induces cell death by caspase-dependent and p38 MAPK pathway in EGFR mutant lung cancer cells: Eun Jin Lim, Jeunghoon Heo, Young-Ho Kim; Kosin Med J. 2016;31(1):30-40. Published online February 4, 2016; DOI: https://doi.org/10.7180/kmj.2016.31.1.30

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Abstract Objectives

The aim of this study was whether quercetin induces cell death by caspase and MAPK signaling pathway in EGFR mutant lung cancer cells

Methods

PC-9 cells, EGFR mutant lung cancer cells, were treated various times and concentrations of quercetin and harvested and measured using MTT assay, DNA fragmentation, Western blotting, and FACS analysis.

Results

Treatment with quercetin in PC-9 cells resulted in inhibition of cell growth through apoptosis. Quercetin-induced apoptosis was associated with caspase-dependent manner. Quercetin also significantly increased levels of phosphor-p38 and decreased levels of phosphor-ERK, indicating that quercetin induces p38 MAPK signaling pathway in PC-9 cells. Quecetin treatment also generated the release of cytochrome c in PC-9 cells; however, pretreatment with rotenone or z-LEHD-fmk, significantly attenuated quercetin-induced apoptosis.

Conclusions

Our data indicate that quercetin exhibits EGFR mutant lung cancer effects through apoptosis by caspase dependent and mitochondrial pathway.

Citations

Citations to this article as recorded by

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Haolin CHU, Shanshan LIU, Shujing ZHANG, Shuyan WANG, Hongsheng CHANG, Lina LI
Chinese Journal of Analytical Chemistry.2024; 52(5): 100397. CrossRef
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Farhad Sheikhnia, Ahmad Fazilat, Vahid Rashidi, Bita Azizzadeh, Mahya Mohammadi, Hossein Maghsoudi, Maryam Majidinia
Pathology - Research and Practice.2024; 260: 155374. CrossRef
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Evidence-Based Complementary and Alternative Medicine.2021; 2021: 1. CrossRef

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