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Search Results: 1 - 10 of 10849 matches for " Sung-Hwan Park "
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Complex System Analysis of Social Networks Extracted from Literary Fictions
Gyeong-Mi Park,Sung-Hwan Kim,Hye-Ryeon Hwang,Hwan-Gue Cho
International Journal of Machine Learning and Computing , 2013, DOI: 10.7763/ijmlc.2013.v3.282
Abstract: Recently we witnessed that the social network analysis focusing on social entities is applied in the social science and web-science, behavioral sciences, as well as in economics, marketing. In this paper we present one method to construct the social network from literary fictions by a simple lexical analysis, not using the complex natural language processing tools. And we will show that those social graphs, saying literary social graph, shows the power law distribution of some features, which is the typical characteristics of complex systems. We showed that the social network extracted from literary data reflects the similar network structure which was semantically designed by authors of fictions. And we newly proposed the concept of the kernel of literary social network by which we can classify the abstract level of protagonists appeared in fictions. Our study shows that the metric distance among characters written in linear text is very similar to the intrinsic and semantic relationship described by fiction writers, which implies the proposed social network from fictions could be another representation of literary fiction. So we can apply other scientific and quantitative approach by analyzing the concrete social graph model extracted from textual data.
Pregnancy Outcomes and Appropriate Timing of Pregnancy in 183 pregnancies in Korean Patients with SLE
Hyun Sun Ko, Hyun Young Ahn, Dong Gyu Jang, Sae-Kyung Choi, Yong-Gyu Park, In Yang Park, Guisera Lee, Sung-Hwan Park, Jong Chul Shin
International Journal of Medical Sciences , 2011,
Abstract: This study was undertaken to investigate the pregnancy outcomes in patients with systemic lupus erythematosus (SLE) and the appropriate timing of pregnancy. We performed a retrospective evaluation of 183 pregnancies with SLE at Catholic University Medical Center during the 13-year period from 1998 to 2010. Pregnancy outcomes were compared according to SLE characteristics. The predictive value of the different cut-off points of the stable period before conception on adverse pregnancy outcomes was calculated by ROC (Receiver operating characteristics) curve analysis. In multivariate analysis, the presence of antiphospholipid antibodies (aPLs) increased the risk of pregnancy loss (p<0.0001) and premature birth (p=0.0040). Active disease at conception increased the risk of premature birth (p< 0.0001) and complications (IUGR, PIH, or both) (p= 0.0078). The other predictor of complications was found to be lupus flare (p=0.0252). At a cut-off level of stable period of 4 months before conception, sensitivity and specificity were 70.8% and 53.2%, 71.4% and 61.5%, and 63.6 % and 59.8 %, respectively on reducing pregnancy loss, premature birth, and complications. Pregnancies with aPLs, active disease at conception and SLE flares are at a higher risk of adverse outcomes. It is essential that disease activity remains stable at least 4 months before conception, for favorable pregnancy outcomes.
Increased interleukin-17 production via a phosphoinositide 3-kinase/Akt and nuclear factor κB-dependent pathway in patients with rheumatoid arthritis
Kyoung-Woon Kim, Mi-La Cho, Mi-Kyung Park, Chong-Hyeon Yoon, Sung-Hwan Park, Sang-Heon Lee, Ho-Youn Kim
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1470
Abstract: Rheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects.IL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the den
Elevated matrix metalloproteinase-9 in patients with systemic sclerosis
Wan-Uk Kim, So-Youn Min, Mi-La Cho, Kyung-Hee Hong, Yong-Joo Shin, Sung-Hwan Park, Chul-Soo Cho
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1454
Abstract: Systemic sclerosis (SSc) is a generalized disorder of connective tissue characterized by microvacular damage and excessive fibrosis in the skin and internal organs, including the heart, lungs, and gastrointestinal tract. One of the major hallmarks of the disease is an increased amount of collagen deposits in the affected tissue. The relative proportion of two major types of skin procollagen, types I and III, is higher in SSc lesions than in healthy controls [1,2]. This increase in collagen deposits may be associated with changes in the dermal microvasculature in SSc. In particular, alterations in the structure of the basement membrane, a critical component of the vessel, may lead to changes in the surrounding tissue and to subsequent development of fibrosis in SSc [3]. The finding that the synthesis of type IV collagen, a major collagen type in basement membrane, is disproportionately increased in the dermal fibroblasts and sera of patients with SSc supports this notion [4,5].The enhanced expression of matrix collagen is presumably associated with abnormal immune responses to collagen in SSc [6-10]. For example, autoantibodies to type IV collagen have been observed in some SSc patients and may be involved in endothelial injury [7,8]. Immunization of mice with autologous type IV collagen leads to the activation of fibroblasts and to fibrosis [9]. Furthermore, type IV collagen activates T cells from patients with SSc [10], suggesting that the selective immunity to type IV collagen may influence the clinical expression of SSc. The excessive production of type IV collagen and subsequent autoimmune T-cell responses to type IV collagen may set off a self-perpetuating cycle in SSc through the interaction between lymphocytes and fibroblasts.The matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases that selectively degrade the components of various extracellular matrixes. Of these, MMP-9 (92–96 kD gelatinase B), whose substrates include type IV collag
Development of a Xeno-Free Autologous Culture System for Endothelial Progenitor Cells Derived from Human Umbilical Cord Blood
Sung-Hwan Moon, Sun-Mi Kim, Soon-Jung Park, Hojin Kim, Daekyeong Bae, Yong-Soo Choi, Hyung-Min Chung
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0075224
Abstract: Despite promising preclinical outcomes in animal models, a number of challenges remain for human clinical use. In particular, expanding a large number of endothelial progenitor cells (EPCs) in vitro in the absence of animal-derived products is the most critical hurdle remaining to be overcome to ensure the safety and efficiency of human therapy. To develop in vitro culture conditions for EPCs derived from human cord blood (hCB-EPCs), we isolated extracts (UCE) and collagen (UC-collagen) from umbilical cord tissue to replace their animal-derived counterparts. UC-collagen and UCE efficiently supported the attachment and proliferation of hCB-EPCs in a manner comparable to that of animal-derived collagen in the conventional culture system. Our developed autologous culture system maintained the typical characteristics of hCB-EPCs, as represented by the expression of EPC-associated surface markers. In addition, the therapeutic potential of hCB-EPCs was confirmed when the transplantation of hCB-EPCs cultured in this autologous culture system promoted limb salvage in a mouse model of hindlimb ischemia and was shown to contribute to attenuating muscle degeneration and fibrosis. We suggest that the umbilical cord represents a source for autologous biomaterials for the in vitro culture of hCB-EPCs. The main characteristics and therapeutic potential of hCB-EPCs were not compromised in developed autologous culture system. The absence of animal-derived products in our newly developed in vitro culture removes concerns associated with secondary contamination. Thus, we hope that this culture system accelerates the realization of therapeutic applications of autologous hCB-EPCs for human vascular diseases.
Curcumin Attenuates Acute Graft-versus-Host Disease Severity via In Vivo Regulations on Th1, Th17 and Regulatory T Cells
Min-Jung Park, Su-Jin Moon, Sung-Hee Lee, Eun-Ji Yang, Jun-Ki Min, Seok-Goo Cho, Chul-Woo Yang, Sung-Hwan Park, Ho-Youn Kim, Mi-La Cho
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067171
Abstract: Background In this study we examined the in vivo and in vitro effects and mechanisms of action of curcumin on the development of acute graft-versus-host disease (GVHD) using a murine model. Methodology/Principal Findings Mixed lymphocyte reactions were used to determine the in vitro effects of curcumin. Treatment with curcumin attenuated alloreactive T cell proliferation and inhibited the production of interferon (IFN)-γ and interleukin (IL)-17. In a murine acute GVHD model, transplantation of curcumin-treated allogeneic splenocytes into irradiated recipient mice significantly reduced the clinical severity scores of acute GVHD manifested in the liver, skin, colon and lung as compared with animals receiving vehicle-treated splenocytes. c-Fos and c-Jun expression levels in the skin and intestine, which are major target organs, were analyzed using immunohistochemical staining. Expression of both proteins was reduced in epithelial tissues of skin and intestine from curcumin-treated GVHD animals. The IFN-γ-expressing CD4+ splenocytes and IFN-γ-expressing lymph node cells were dramatically decreased in curcumin-treated mice. In contrast, CD4+Foxp3+ splenocytes were increased in the curcumin-treated acute GVHD animals. Flow cytometric analysis revealed that animals transplanted with curcumin-treated allogeneic splenocytes showed increased populations of CD4+ regulatory T cells (Tregs) as well as CD8+ Treg cells, compared to animals administered vehicle-treated splenocytes. Curcumin-treated acute GVHD animals could have a change in B cell subpopulations. Conclusion/Significance In the present study, we investigated the efficacy and mechanism of action of curcumin treatment against acute GVHD. The acute GVHD mice administered with curcumin-treated splenocytes showed significantly reduced severity of acute GVHD. Curcumin exerted in vivo preventive effects on acute GVHD by reciprocal regulation of T helper 1 (Th1) and Treg (both CD4+ and CD8+ Treg) cell lineages as well as B cell homeostasis.
TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in patients with primary Sjogren's syndrome
Seung-Ki Kwok, Mi-La Cho, Yang-Mi Her, Hye-Joa Oh, Mi-Kyung Park, Seon-Yeong Lee, Yun Woo, Ji Ju, Kyung-Su Park, Ho-Youn Kim, Sung-Hwan Park
Arthritis Research & Therapy , 2012, DOI: 10.1186/ar3780
Abstract: The expressions of various TLRs, IL-17 and the cytokines involved in Th17 cell differentiation including IL-6, IL-23, tumor necrosis factor-alpha (TNF-α) and IL-1β were examined by immunohistochemistry in salivary glands of pSS patients. The IL-17 producing CD4+ T cells (Th17 cells) were examined by flow cytometry and confocal staining in peripheral mononuclear blood cells (PMBCs) and salivary glands of pSS patients. After PBMCs were treated with TLR specific ligands, the induction of IL-17 and IL-23 was determined using real-time PCR and ELISA. The signaling pathway that mediates the TLR2 stimulated production of IL-17 and IL-23 was investigated by using treatment with specific signaling inhibitors.We showed that TLR2, TLR4, TLR6, IL-17 and the cytokines associated with Th17 cells were highly expressed in salivary glands of pSS patients but not in controls. The expressions of TLR2, TLR4 and TLR6 were observed in the infiltrating mononuclear cells and ductal epithelial cells, whereas IL-17 was mainly observed in infiltrating CD4+ T cells. The number of IL-17 producing CD4+ T cells was significantly higher in pSS patients both in PBMCs and minor salivary glands. The stimulation of TLR2, TLR4 and TLR6 additively induced the production of IL-17 and IL-23 from the PBMCs of pSS patients especially in the presence of TLR2 stimulation. IL-6, signal transducer and activator of transcription 3 (STAT3) and nuclear factor-kappaB (NF-kB) pathways were implicated in the TLR2 stimulated IL-17 and IL-23.Our data demonstrate that TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in pSS. Therefore, therapeutic strategies that target TLR/IL-17 pathway might be strong candidates for treatment modalities of pSS.Sj?gren's syndrome (SS) is a relatively common autoimmune exocrinopathy that is associated with infiltration of lymphocytes and is characterized by gradually progressive lachrymal and salivary dysfunction [1,2]. The exocrine dysfunction can oc
Impact of interleukin-21 in the pathogenesis of primary Sjogren's syndrome: increased serum levels of interleukin-21 and its expression in the labial salivary glands
Kwi Kang, Hyun-Ok Kim, Seung-Ki Kwok, Ji Ju, Kyung-Su Park, Dong-Il Sun, Joo Jhun, Hye Oh, Sung-Hwan Park, Ho-Youn Kim
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3504
Abstract: Serum IL-21 levels in 40 primary SS, 40 rheumatoid arthritis (RA), and 38 systemic lupus erythematosus (SLE) patients and 20 healthy controls were measured. Serum IL-21 levels of SS patients were assessed for correlations with laboratory data, including anti-nuclear antibody, anti-Ro/La antibodies, globulin, immunoglobulin (Ig) class, and IgG subclass. LSGs from 16 primary SS and 4 controls with sicca symptoms were evaluated for IL-21 and IL-21 receptor (IL-21R) expression by immunohistochemistry. Confocal microscopy was performed to further characterize the IL-21 positive cells.Primary SS patients had significantly higher serum IL-21 levels than controls, and these increments correlated positively with levels of IgG, IgG1. Serum IgG1 levels correlated with anti-Ro antibody titers. Immunohistochemical analyses showed that lymphocytic foci and the periductal area of the LSGs from SS patients expressed high levels of IL-21 and lower levels of IL-21R, whereas the control LSGs showed minimal expression of both antigens. The more the lymphocyte infiltrated, IL-21expression in LSGs showed a tendency to increase. Confocal microscopic analyses revealed that IL-21 expressing infiltrating lymphocytes in the LSGs of SS patients also expressed CXCR5.Primary SS is associated with high serum IL-21 levels that correlate positively with serum IgG, especially IgG1, levels. The expression of IL-21 is increased as more lymphocytes infiltrated in LSGs. These observations suggest that IL-21 may play an important role in primary SS pathogenesis.IL-21 is a pleiotropic cytokine that belongs to the common cytokine receptor γ chain (γc)-dependent cytokine family, which is produced by activated CD4+ T cells and NKT cells [1]. The IL-21 receptor (IL-21R) consists of the IL-21R α chain and the γc chain and is expressed on T cells, NK cells, NKT cells, B cells, dendritic cells (DCs) and macrophages as well as on non-hematopoietic cells, including keratinocytes and fibroblasts [2]. The activation
Dysfunctional interferon-α production by peripheral plasmacytoid dendritic cells upon Toll-like receptor-9 stimulation in patients with systemic lupus erythematosus
Seung-Ki Kwok, June-Yong Lee, Se-Ho Park, Mi-La Cho, So-Youn Min, Sung-Hwan Park, Ho-Youn Kim, Young-Gyu Cho
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2382
Abstract: The concentrations of IFN-α were determined in serum and culture supernatant of peripheral blood mononuclear cells (PBMCs) from SLE patients and healthy controls after stimulation with CpG ODN2216 or SLE serum. The numbers of circulating pDCs were analyzed by fluoresence-activated cell sorting analysis. pDCs were treated with CpG ODN2216 and SLE serum repeatedly, and levels of produced IFN-α were measured. The expression of IFN-α signature genes and inhibitory molecules of TLR signaling were examined in PBMCs from SLE patients and healthy control individuals.Although there was no significant difference in serum concentration of IFN-α and number of circulating pDCs between SLE patients and healthy control individuals, the IFN-α producing capacity of PBMCs was significantly reduced in SLE patients. Interestingly, the degree which TLR9 ligand-induced IFN-α production in SLE PBMCs was inversely correlated with the SLE serum-induced production of IFN-α in healthy PMBCs. Because repeated stimulation pDCs with TLR9 ligands showed decreased level of IFN-α production, continuous TLR9 stimulation may lead to decreased production of IFN-α in SLE PBMCs. In addition, PBMCs isolated from SLE patients exhibited higher expression of IFN-α signature genes and inhibitory molecules of TLR signaling, indicating that these cells had already undergone IFN-α stimulation and had become desensitized to TLR signaling.We suggest that the persistent presence of endogenous IFN-α inducing factors induces TLR tolerance in pDCs of SLE patients, leading to impaired production of IFN-α.Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is characterized by generation of autoantibodies against nuclear DNA and/or nuclear proteins [1]. The precise pathogenesis of SLE remains unknown, but both genetic and environmental factors are involved [2]. Over the past two decades numerous studies have suggested that interferon (IFN)-α may play a pathogenic role in SLE. This view is derived fr
Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
Uk Moon, Su Park, Sang Oh, Wan-Uk Kim, Sung-Hwan Park, Sang-Heon Lee, Chul-Soo Cho, Ho-Youn Kim, Won-Keun Lee, Suk Lee
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1181
Abstract: Systemic lupus erythematosus (SLE) is an idiopathic disease characterized by variable inflammatory destruction. A variety of autoantibodies are found in the serum of SLE patients, indicating that SLE is an autoimmune disease [1]. However, the mechanisms that lead to the aberrant autoimmune responses are not clearly understood, and various genetic and environmental factors are thought to be involved [2]. Epstein–Barr virus (EBV) is suspected to play a role in predisposing to SLE for several reasons. First, EBV promotes proliferation of B cells after infection, and thus it poses a prolonged antigenic challenge. This prolonged EBV antigen expression may trigger SLE in genetically prone individuals. Second, EBV-infected B cells can become a continuous source of autoantibodies. Third, sequence homologies exist between SLE autoantigens and some EBV proteins, such as EBV nuclear antigen (EBNA)-1 and EBNA-2. The antibodies elicited by these viral antigens may cross-react with autoantigens and trigger SLE [3-5].If EBV is indeed involved in the pathogenesis of SLE, then there must be some association between EBV infection and SLE [6-9]. Elevated titers of anti-EBV antibodies have been detected in SLE patients compared with control individuals [10-12]. It is difficult to prove that there is any association between EBV and SLE by comparing seroconversion rates between patients and healthy control individuals because the majority of adults are seropositive for EBV [13]. Recently, James and coworkers [14,15] examined more than 100 SLE patients and found that the EBV seroconversion rate was significantly greater in SLE patients than in normal control individuals, both in young and adult populations. However, these studies do not prove the existence of a temporal relationship between EBV infection and development of SLE. In addition, measuring antibodies to EBV antigen does not directly indicate the status of EBV within the body. This is because the serologic response can be affect
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