Youn Jung Kim

Prof. Youn Jung Kim

College of Nursing Science, Kyung Hee University
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Research Focus & Metrics

Academic Career Length

20Years (2007-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2017 in Neuroscience Letters
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Journal Article
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JLJae-Min Lee
Jae-Min Lee
JPJong-Min Park
Jong-Min Park
MSMin Kyung Song
Min Kyung Song
YOYoo Joung Oh
Yoo Joung Oh
CKChang-Ju Kim
Chang-Ju Kim
YKYoun Jung Kim
Youn Jung Kim

1 August 2021 in Physiology & Behavior
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Journal Article
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MSMin Kyung Song
Min Kyung Song
JLJoo Hee Lee
Joo Hee Lee
YKYoun Jung Kim
Youn Jung Kim
Adolescence is a critical period of establishing social relations through social interactions that affect the emotional development associated with stress responses, anxiety, depression, and cognitive development. We investigated the behavioral and neurobiological changes induced by handling and social isolation in adolescent rats to determine social interaction effects. Rats were randomly divided into groups and used as a control, a handling, and a social isolation group. After 12 weeks, the handling group showed a significant increase in mobility in the open field test and in tryptophan hydroxylase expression in the dorsal raphe nucleus, as well as significantly reduced immobility times in the forced swim test, compared to the control group (p < 0.05). The social isolation group, in contrast, showed a significant increase in immobility times in the forced swim test and in glucocorticoid and SIRT1 expression in the hippocampus, as well as a significant reduction in mobility in the open field test and in escape latency times in the passive avoidance test, compared to the control group (p < 0.05). The present results show that while handling did not improve cognitive function, it reduced anxiety and lowered depression levels; social isolation, in contrast, significantly impaired the animals' stress response, anxiety and depression levels, and cognitive function. Our findings indicate that handling and social isolation have a strong effect on adolescents' emotional and cognitive development into healthy adults.

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JLJae Min Lee
Jae Min Lee
JLJoo-Hee Lee
Joo-Hee Lee
MSMin-Kyung Song
Min-Kyung Song
YKYoun Jung Kim
Youn Jung Kim
Vascular dementia (VaD) is a progressive cognitive impairment caused by a reduced blood supply to the brain. Chronic cerebral hypoperfusion (CCH) is one cause of VaD; it induces oxidative stress, neuroinflammation, and blood-brain barrier (BBB) disruption, damaging several brain regions. Vitamin C plays a vital role in preventing oxidative stress-related diseases induced by reactive oxygen species, but it is easily oxidized and loses its antioxidant activity. To overcome this weakness, we have developed a vitamin C/DNA aptamer complex (NXP031) that increases vitamin C’s antioxidant efficacy. Aptamers are short single-stranded nucleic acid polymers (DNA or RNA) that can interact with their corresponding target with high affinity. We established an animal model of VaD by permanent bilateral common carotid artery occlusion (BCCAO) in 12 week old Wistar rats. Twelve weeks after BCCAO, we injected NXP031 into the rats intraperitoneally for two weeks at moderate (200 mg/4 mg/kg) and high concentrations (200 mg/20 mg/kg). NXP031 administration alleviates cognitive impairment, microglial activity, and oxidative stress after CCH. NXP031 increased the expression of basal lamina (laminin), endothelial cell (RECA-1, PECAM-1), and pericyte (PDGFRβ); these markers maintain the BBB integrity. We found that NXP031 administration activated the Nrf2-ARE pathway and increased the expression of SOD-1 and GSTO1/2. These results suggest that this new aptamer complex, NXP031, could be a therapeutic intervention in CCH-induced VaD.

1 April 2014 in Journal of Ginseng Research
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SLSena Lee
Sena Lee
MKMyung-Gyou Kim
Myung-Gyou Kim
SKSung Kwon Ko
Sung Kwon Ko
HKHye Kyung Kim
Hye Kyung Kim
KLKang Hyun Leem
Kang Hyun Leem
YKYoun Jung Kim
Youn Jung Kim
The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.

31 December 2010 in International Neurourology Journal
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MBMohammad Iqbal Hossain Bhuiyan
Mohammad Iqbal Hossain Bhuiyan
YKYoun Jung Kim
Youn Jung Kim
Bhuiyan MI, et al. Int Neurourol J. 2010 Dec;14(4):203-212. http://dx.doi.org/10.5213/inj.2010.14.4.203

7 March 2014 in BMC Complementary and Alternative Medicine
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HKHee Kang
Hee Kang
SPSung-Hyun Park
Sung-Hyun Park
JYJeong-Moon Yun
Jeong-Moon Yun
TNTae Gyu Nam
Tae Gyu Nam
YKYoung-Eun Kim
Young-Eun Kim
YKYoun Jung Kim
Youn Jung Kim
Water soluble cinnamon extract has been shown to increase insulin sensitivity and modulate macrophage activation, a desirable trait for the management of obesity or atherosclerosis. Our present study investigated whether cinnamon water extract (CWE) may influence the differentiation of monocytes into macrophages and the activity of macrophage scavenger receptors, commonly observed in atherosclerotic lesions.