The Influence of Western Culture on Health in Asian Countries

Park, Yongsoo,Lee, Jae Ung Medical Publications Korea 1997 Medical Progress Vol.19 No.1

South Korea’s Hedging toward South Korea-United States-China Trilateral Dynamics

YongSoo Park 미래사회통합연구센터 2021 Journal of Conflict and Integration Vol.5 No.1

Despite increasing domestic and international pressure to choose between the US Indo-Pacific Strategy and China"s Belt and Road Initiative, South Korea is still not officially participating in either of the two countries’ core strategies. Instead, South Korea introduced a neutral policy called the New Southern Policy. Through the New Southern Policy, South Korea has been encouraging participation by strategic functions in areas that have a common interest between South Korea, the United States, and China, and has been promoting and reinforcing cooperation with the two superpowers simultaneously. This ambiguous strategy taken by South Korea is a typical hedging strategy that the weaker state takes against the competing two great powers while maintaining a certain distance from the fierce competition between them. This shows that a hedging strategy asserted in the balance of power theory is valid in explaining the strategic actions South Korea is taking in relation to the fierce US-China competition in the Indo-Pacific region of the 21st century.

Oxidative stress, mitochondrial dysfunction and endoplasmic reticulum stress

Yongsoo Park 한국구조생물학회 2014 Biodesign Vol.2 No.1

Diabetes mellitus is a chronic complex metabolic condition that affects carbohydrate, lipid and protein metabolism and may impair numerous organs and functions of the organism. Hyperglycemia is only the most obvious biochemical marker of diabetes, and the main contributor to the development of diabetes complications is the cumulative effect of chronic hyperglycemia. Increasing evidence suggests that oxidative stress may be the key mediators of the deleterious effects of hyperglycemia. Mitochondria play a central role in the generation of reactive oxygen species and cell apoptosis. A number of conditions including nutrient excess that interfere with proper endoplasmic reticulum (ER) function may lead accumulation of unfolded proteins, which then trigger apoptotic as well as adaptive downstream signaling pathways. Many studies have also provided ample evidences that mitochondrial dysfunction and ER stress are most important pathogenic causes for the development of diabetes and its complications. Regulation mechanisms of how mitochondria play in the metabolism of glucose and fatty acids, the primary fuels used by cells to produce ATP, have been the subject of tremendous interests. Nonetheless, much remains to be investigated such as tissue-specific fuel selection and its relation with the pathogenesis of diabetes and complications. Cellular homeostasis depends upon the functional relationship between mitochondria and the ER. Propagation of calcium signaling from ER to mitochondria is involved in both ATP production and cell death. On the other hand, the ER requires ATP to function properly, which may make it the best site for sensing metabolic stress. In this article, oxidative stress, mitochondrial dysfunction and ER stress, especially their realtime interaction in diabetes and complication development will be reviewed.

The HOOK region of voltage-gated Ca ²⁺ channel β subunits senses and transmits PIP ₂ signals to the gate

Park, Cheon-Gyu,Park, Yongsoo,Suh, Byung-Chang The Rockefeller University Press 2017 The Journal of general physiology Vol.149 No.2

<P>The β subunit of voltage-gated Ca<SUP>2+</SUP> (Ca<SUB>V</SUB>) channels plays an important role in regulating gating of the α1 pore-forming subunit and its regulation by phosphatidylinositol 4,5-bisphosphate (PIP<SUB>2</SUB>). Subcellular localization of the Ca<SUB>V</SUB> β subunit is critical for this effect; N-terminal–dependent membrane targeting of the β subunit slows inactivation and decreases PIP<SUB>2</SUB> sensitivity. Here, we provide evidence that the HOOK region of the β subunit plays an important role in the regulation of Ca<SUB>V</SUB> biophysics. Based on amino acid composition, we broadly divide the HOOK region into three domains: S (polyserine), A (polyacidic), and B (polybasic). We show that a β subunit containing only its A domain in the HOOK region increases inactivation kinetics and channel inhibition by PIP<SUB>2</SUB> depletion, whereas a β subunit with only a B domain decreases these responses. When both the A and B domains are deleted, or when the entire HOOK region is deleted, the responses are elevated. Using a peptide-to-liposome binding assay and confocal microscopy, we find that the B domain of the HOOK region directly interacts with anionic phospholipids via polybasic and two hydrophobic Phe residues. The β2c-short subunit, which lacks an A domain and contains fewer basic amino acids and no Phe residues in the B domain, neither associates with phospholipids nor affects channel gating dynamically. Together, our data suggest that the flexible HOOK region of the β subunit acts as an important regulator of Ca<SUB>V</SUB> channel gating via dynamic electrostatic and hydrophobic interaction with the plasma membrane.</P>

TGFβ Plasmid Construction and Delivery for the Prevention of Type 1 Diabetes

Park, Leejin,Lee, Eunjig,Lee, Sangkyung,Lim, Minsu,Hong, Hekyung,Shin, Geewook,Park, Yongsoo Wiley (New York Academy of Sciences) 2008 Annals of the New York Academy of Sciences Vol.1150 No.1

<P>Studies of animals with spontaneous autoimmune diabetes have revealed that autoreactive T cells that mediate islet beta cell destruction can be manipulated by the administration of Th(2) cytokines. Using gene delivery to express the targeted protein, we can overcome the need for frequent administration of cytokines on account of their short half-lives. In this study, the effect of hTGFbeta gene delivery was evaluated both in vitro and in vivo using an adenovirus vector (Ad) constructed with an hTGFbeta cDNA. In vitro transfection assays of the construct in HepG2, beta cell lines, and islets showed good expression levels of hTGFbeta and activation of smad3. Ad-hTGFbeta enhanced differentiation and proliferation in the beta cell line or islets without causing apoptosis. Of interest, Ad-hTGFbeta transduction in CD4(+)CD25(-) T cells resulted in a significant enhanced expression of CD25 and a regulatory T cell-specific transcription factor, Foxp3. To evaluate in vivo efficacy, Ad-hTGFbeta was intravenously injected into 7-week-old NOD mice and compared to the transduction using the vector only. The Ad-hTGFbeta group had persistent gene expression for longer than 5 weeks, and high TGFbeta serum level was secreted. There was no difference in the degree of insulitis between the Ad-hTGFbeta group and controls. Although we found favorable in vitro results, such as decrease in islet apoptosis, enhanced proliferation and differentiation, and increase in the level of CD4(+)CD25(+) regulatory T cells, there was no difference in reduction of the development of T1D between controls and Ad-hTGFbeta-injected mice. Nevertheless, if we find the appropriate mode and timing of TGFbeta gene transduction, Ad-hTGFbeta gene therapy might be useful in therapeutic cytokine delivery for the treatment of T1D.</P>

Type 1 diabetes genetic susceptibility markers and their functional implications

Park, Yongsoo Korean Society of Medical Genetics and Genomics 2014 대한의학유전학회지 Vol.11 No.1

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by selective destruction of pancreatic ${\beta}$-cells resulting in insulin deficiency. The genetic determinants of T1D susceptibility have been linked to several loci, in particular to the human leukocyte antigen (HLA) region, which accounts for 50% of the genetic risk of developing T1D. Multiple genes in the HLA region, which are in strong linkage disequilibrium, are thought to be involved. Another important locus, with a smaller effect on genetic predisposition to T1D, is the insulin gene. The advent of numerous single nucleotide polymorphism markers and genome screening has enabled the identification of dozens of new T1D susceptibility loci. Some of them appear to predispose to T1D independently of the HLA and may be important in families with T1D who lack strong HLA susceptibility. Other loci may interact with each other to cause susceptibility. The autoimmune response against ${\beta}$-cells can also be triggered by environmental factors in the presence of a predisposing genetic background. Deciphering the environmental and genetic factors involved should help to understand the origin of T1D and aid in the design of individualized prevention programs.

Effects of Temperature and Humidity Treatment Conditions on the Interfacial Adhesion Energy between the Electroless-Plated Ni and Polyimide

Park, Sung-Cheol,Min, Kyoung-Jin,Lee, Kyu Hwan,Jeong, Yongsoo,Park, Young-Bae IOP Publishing 2010 Japanese journal of applied physics Vol.49 No.8

Dominant role of lipid rafts L-type calcium channel in activity-dependent potentiation of large dense-core vesicle exocytosis

Park, Yongsoo,Kim, Kyong-Tai Blackwell Publishing Ltd 2009 Journal of Neurochemistry Vol.110 No.2

<P>Abstract</P><P>Calcium influx triggers exocytosis by promoting vesicle fusion with the plasma membrane. However, different subtypes of voltage-gated calcium channel (VGCC) have distinct roles in exocytosis. We previously reported that repetitive stimulation induces activity-dependent potentiation (ADP) which represents the increase of neurotransmitter release. Here, we show that L-type VGCC have a dominant role in ADP of large dense-core vesicle (LDCV) exocytosis. Repetitive stimulation activating VGCC can induce ADP, whereas activation of bradykinin (BK) G protein-coupled receptors or purinergic P2X cation channels can not. L-type VGCC has the dominant role in ADP of LDCV exocytosis by regulating Protein Kinase C (PKC)-epsilon translocation and phosphorylation of myristoylated alanine-rich C kinase substrate (MARCKS), a target molecule of PKC-epsilon. We provide evidence that L-type VGCC, PKC-epsilon, and MARCKS, but not Q-type VGCC, are selectively located in lipid rafts. Also, PKC-epsilon translocation induced by L-type VGCC activation occurs in lipid rafts. Disruption of lipid rafts abolishes ADP of LDCV exocytosis and changes the fusion pore kinetics without affecting the first stimulation-induced exocytosis, showing that lipid rafts are involved in the potentiation process. Taken together, we suggest that L-type VGCC in lipid rafts selectively mediates ADP of LDCV exocytosis by regulating PKC-epsilon translocation and MARCKS phosphorylation.</P>

Comparison of SVM and RF Classifiers for Stress and Fatigue Recognition

Yungi Park,Yongsoo Park,Youn-Sung Lee,Jeongwook Seo 한국정보통신학회 2018 2016 INTERNATIONAL CONFERENCE Vol.10 No.1

RTV 도포부 가스패스 제거공정 연구

박용수(Yongsoo Park),이상진(Sangjin Lee),김성수(Sungsoo Kim),탁효성(Hyosung Tak),백기봉(Kibong Baek),박민수(Minsoo Park),노영희(Younghee Roh) 한국추진공학회 2022 한국추진공학회 학술대회논문집 Vol.2022 No.11