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      • Interleukin-1B(1L-1B) polymorphisms and gastric mucosal levels of IL-Iβ cytokine in Korean patients with gastric cancer

        Chang, Young-Woon,Jang, Jae-Young,Kim, Nam-Hoon,Lee, Jae Won,Lee, Hyo Jung,Jung, Woon Won,Dong, Seok-Ho,Kim, Hyo-Jong,Kim, Byung-Ho,Lee, Joung-Il,Rin Chang KYUNG HEE UNIVERSITY MEDICAL CENTER 2006 고황의학상 수상논문집 Vol.21-22 No.-

        Interleukin-1B and IL-1 receptor antagonist gene polymorphisms are associated with an increased risk of gastric cancer (GC) in Caucasian populations. However, recent studies could not find any association between IL-1B-511T polymorphism and the risk of GC in Asians. We tested for an association between IL-1 loci polymorphisms with increased gastric mucosal levels of IL-1β and an increased risk of developing GC in a Korean population. Polymorphisms of IL-1A-889, IL-1B-31, IL-1B-511 and IL-1RN were genotyped in 434 controls and 234 patients with GC. Mucosal IL-1β cytokine was measured using an ELISA. The frequencies of IL-1A, IL-1B-511, IL-1B-31 and IL-1RN were not statistically different between controls and all patients with GC. After subclassification of GC, only patients with intestinal-type GC showed a higher frequency of IL-1B-31T homozygotes (OR = 2.2; 95% CI = 1.1-4.3) compared with controls. Risk was also significantly increased in these patients for IL-1B-31T homozygotes compared with patients with diffuse-type GC (OR = 3.4; 95% CI = 1.5-7.7). As in Caucasian populations, linkage disequilibrium between IL-1B-31 and IL-1B-511 was nearly complete, but the pattern of haplotype related to the risk of GC (IL-1B-31T/IL-1B-511C) was opposite (IL-1B-511T/IL-1B-31C). Mucosal IL-1β levels in H. pylori-infected GC patients were higher in patients homozygous for IL-1B-31T compared with IL-1B-31C/T and IL-1B-31C/C. Thus, the combined effects of H. pylori infection and IL-1B-31T/IL-1B-511C polymorphisms with enhanced mucosal IL-1β production contributed to the development of intestinal-type GC in this Korean population.

      • KCI등재

        Interleukin-17이 배양된 류마티스관절염 활막세포에서 vascular endothelial growth factor 생성에 미치는 영향

        곽임수 ( Ihm Soo Kwak ),남태수 ( Tae Soo Nam ),나하연 ( Ha Yeon Rha ),서정탁 ( Jeung Tak Suh ),김유선 ( Yoo Sun Kim ),김성일 ( Sung Il Kim ) 대한류마티스학회 2001 대한류마티스학회지 Vol.8 No.3

        Objective: To investigate the the effects of interleukin-17 (IL-17) on the production of vascular endothelial growth factor (VEGF) from cultured rheumatoid arthritis synoviocytes. Methods: Fibroblast-like synovial cells(FLS) were prepared from the synovial tissues of rheumatoid arthritis patients and cultured in the presence of IL-17, IL-17 with or without transforming growth factor-β(TGF-β), tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β). VEGF levels were determined in the culture supernatants by sandwitch ELISA. Results: Stimulation of FLS by serial concentration of IL-17, TGF-β, TNF-α, IL-1β increased the production of VEGF by 2.1-2.7, 2.2-3.0, 2.0-2.9, 2.3-3.1 fold over the constitutive levels of unstimulated FLS. Stimulation of FLS by IL-17 with TGF-β or TNF-α or IL-1β also increased the production of VEGF according to culture periods by 1.6-1.8, 1.1-1.9, 1.5-1.7 fold over the levels stimulated with TGF-β or TNF-α or IL-1β, respectively. This results indicated that IL-17 increased the effect of TGF-β, TNF-α, IL-1β on FLS, leading synergistic enhancement of VEGF production. Conclusion: IL-17 may be involved in the neovascularization in rheumatoid synovitis by enhancing the production of VEGF.

      • KCI등재

        Nam’s Method에 의한 下顎顆頭 및 頸部 骨折 處置 (II)

        Il Woo Nam(南日祐) 대한구강악안면외과학회 1980 대한구강악안면외과학회지 Vol.6 No.1

        It is very difficult that the fractured condylar head and upper condylar neck have to be reduced and immobilized properly. The reduction and fixaton of the fractured those bones are so difficult to be reduced and fixated that many oral surgeons are trying to study on how to operate an adequate reduction and fixation. In spite of endeavor, lots of fragments of the fractured condylar heads frequently have been removed as so-called condylectomies because complexities of the surrounding anatomical structures make adequate reductions and fixations impossible. Thus the author has developed a new method named Dr. Nam s method in terms of oblique osteotomy, interosseous wiring extraorally, and replantation by which I have successfully treated 48 patients with fractures of the condylar head or upper part of the condylar neck of the mandibles since 1976. In order to reduce and immobilize those fractured, firstly, oblique osteotomy at the affected ascending ramus of the mandible was preceded, and secondly, the separated posterior part of the ascendingramus and fractured condylar head were carefully removed out from the body to be reduced and immobilized together extraorally, and lastly, replantations were made at the same sites. The results were drawn as follows: 1. The author successfully has treated 48 patients with the condylar head or upper condylar neck fractures by using Dr. Nam s method. 2. No intermaxillary fixation or less than 1 week intermaxillary wiring was needed after surgery. 3. The normal mouth opening and closing, and facial appearnaces could be observed in 1 month aft er surgery. 4. Traumatic injury for instance, automobile accident, was one of the commonest causes of fractures of the condylar head and upper condylar neck. 5. The features of those fractures were type I; one single fragment of upper condylar neck, Type II ; oblique. single fracture from the inner condylar head to its articular surface, and type III ; fractures with 3 pieces condylar head in the order.

      • SCIESCOPUSKCI등재

        Association of DOCK8, IL17RA, and KLK12 Polymorphisms with Atopic Dermatitis in Koreans

        ( Won Il Heo ),( Kui Young Park ),( Mi-kyung Lee ),( Yu Jeong Bae ),( Nam Ju Moon ),( Seong Jun Seo ) 대한피부과학회 2020 Annals of Dermatology Vol.32 No.3

        Background: Early-onset and severe atopic dermatitis (AD) in patients increase the probability of the development of allergic rhinitis or asthma. Treatment and prevention strategies in infants and young children with AD are targeted toward treating the symptoms, restoring skin barrier functions, and reducing the absorption of environmental allergens in an attempt to attenuate or block the onset of asthma and food allergy. Objective: Given that the initiating events in AD remain poorly understood, identifying those at risk and implementing strategies to prevent AD is necessary. Methods: Whole-exome sequencing (WES) was performed in a 43 control group and a disease group with 20 AD patients without atopic march (AM) and 20 with AM. Sanger sequencing was carried out to validate found variants in cohorts. Results: DOCK8, IL17RA, and KLK12 single-nucleotide polymorphisms were identified by WES as missense mutations: c.1289C>A, p.P97T (rs529208); c.1685C>A, p.P562G (rs12484684); and c.457+27>C, rs3745540, respectively. A case-control study show that total immunoglobulin E (IgE) level was significantly increased in the AA genotype of DOCK8 compared to the CA genotype in allergic patients. The rs12484684 of IL17RA increased risk of adult-onset AD (odds ratio: 1.63) compared to the control for (A) allele frequency. AD and AM Patients with the IL17RA CA genotype also had elevated IgE levels. rs3745540 of KLK12 was associated with AD in dominant model (odds ratio: 2.86). Conclusion: DOCK8 (rs529208), IL17RA (rs12484684), and KLK12 (rs3745540), were identified using a new WES filtering method. the result suggests that polymorphism of DOCK8 and IL17RA might be related to increase the total IgE level. (Ann Dermatol 32(3) 197∼205, 2020)

      • SCIESCOPUSKCI등재

        The Effect of Abdominal Visceral Fat, Circulating Inflammatory Cytokines, and Leptin Levels on Reflux Esophagitis

        ( Su Youn Nam ),( Il Ju Choi ),( Kum Hei Ryu ),( Bum Joon Park ),( Young Woo Kim ),( Hyun Beom Kim ),( Jeongseon Kim ) 대한소화기기능성질환·운동학회 2015 Journal of Neurogastroenterology and Motility (JNM Vol.21 No.2

        Background/Aims Although adipocytes secrete inflammatory cytokines and adipokines, their role in reflux esophagitis is controversial. We investigated the association between visceral fat and inflammatory cytokines or adipokines in reflux esophagitis. Methods Abdominal visceral fat and cytokines were measured in 66 individuals with reflux esophagitis and 66 age- and sex-matched controls. The mean values for visceral fat and cytokines were compared in cases and controls. Second, correlations between visceral fat and inflammatory cytokines were measured. Finally, multiple logistic regression models for odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the effects of visceral fat and cytokines on reflux esophagitis. Results Visceral fat, leptin, interleukin (IL)-6, and IL-1β were higher in reflux esophagitis compared to controls. Visceral fat showed a strong positive correlation with IL-6 (r = 0.523, P < 0.001), IL-8 (r = 0.395, P < 0.001), and IL-1β (r = 0.557, P < 0.001), and a negative correlation with adiponectin (r = -0.466, P < 0.001). With adjusted analysis, visceral fat/100 (OR, 4.32; 95% CI, 2.18-8.58; P < 0.001) and leptin (OR, 1.36; 95% CI, 1.10-1.69; P = 0.005) independently increased the risk of reflux esophagitis, but the effects of other cytokines were abolished. Conclusions Visceral fat may increase the risk of reflux esophagitis by increasing the levels of inflammatory cytokines. Leptin showed a positive association with reflux esophagitis that was independent of visceral fat. (J Neurogastroenterol Motil 2015;21:247-254)

      • SCISCIESCOPUS

        Recovery of ionic liquid and sugars from hydrolyzed biomass using ion exclusion simulated moving bed chromatography

        Mai, Ngoc Lan,Nguyen, Nam Trung,Kim, Jin-Il,Park, Hyuk-Min,Lee, Sung-Kyun,Koo, Yoon-Mo Elsevier 2012 Journal of Chromatography A Vol.1227 No.-

        <P><B>Highlights</B></P><P>► Ionic liquid was successfully separated from aqueous sugar mixtures by ion exclusion SMB. ► Ionic liquid and sugar recovery yield depend on the SMB zone flow rates. ► Complete recovery of ionic liquid could be obtained by optimization of SMB zone configuration.</P> <P><B>Abstract</B></P><P>Efficient recovery of ionic liquid (IL) from aqueous mixture of ILs and sugars (which derived from enzymatic or chemical catalyzed hydrolysis of ILs-pretreated biomass) is a major drawback for commercialization of biofuel and platform chemicals production from biomass utilized ILs as pretreatment solvent. In this study, simulated moving bed (SMB) chromatography equipped with ion exclusion column (containing [Emim]<SUP>+</SUP> cation) was investigated to separate sugars (glucose and xylose) which are the main products from biomass hydrolysate and 1-Ethyl-3-methylimidazolium acetate (EmimAc) which is the ILs used for biomass pretreatment. A four-zone SMB system with a configuration of 2-2-2-2 (2 ion exclusion columns in each zone) was used to recover glucose, xylose and EmimAc from their aqueous mixture with yield of 71.38, 99.37 and 98.92%, respectively. Moreover, the optimization of SMB zone configuration by simulation results in a complete recovery of ILs. This result indicates that for the first time, ion exclusion SMB chromatography could be used for complete recovery of ILs from aqueous sugar mixture.</P>

      • SCIESCOPUSKCI등재

        The Effects of Ketorolac Tromethamine and Baicalein on the Levels of Inflammatory Factors in Human Synoviocytes

        Yang, Jae-Heon,Yun, Mi-Young,Lee, Nam-Hee,Kim, Dae-Keun,Kim, Young-Il,Noh, Young-Hee,Kim, Tae-Youl,Yoon, Se-Won,Shin, Sang-Chul 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.11

        This study examined the effects of ketorolac tromethamine (KT) and baicalein (BE) on the levels of inflammatory factors in human synoviocytes. The fibroblast-like synoviocytes (FLS) cells were used to determine the possible regulatory effects of KT and BE (KTBE) on the levels of inflammatory factors in FLS cells. In addition, the levels of TNF-$\alpha$, IL-6, and IL-$1{\beta}$ mRNA expression in FLS cells induced by a TNF-$\alpha$ and IL-$1{\beta}$ co-treatment were largely inhibited by a KTBE treatment. The level of FLS cells proliferation was increased by IL-$1{\beta}$ and TNF-$\alpha$, and strongly inhibited by KTBE treatment. The production of oxygen species (ROS) was inhibited by KTBE in FLS cells. KTBE appears to regulate the levels of mRNA that are important for regulating RA progression.

      • KCI등재

        Soluble mediators from mesenchymal stem cells suppress T cell proliferation by inducing IL-10

        Seung-Ha Yang,Min-Jung Park,Il-Hee Yoon,Su-Young Kim,So-Hee Hong,Jin-Young Shin,Hye-Young Nam,김용희,Bongi Kim,박정규 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.5

        Mesenchymal stem cells (MSCs) can inhibit T cell proliferation; however, the underlying mechanisms are not clear. In this study, we investigated the mechanisms of the immunoregulatory activity of MSCs on T cells. Irradiated MSCs co-cultured with either naïve or pre-activated T cells in a mixed lymphocyte reaction (MLR) significantly suppressed T cell proliferation in a dose-dependent manner, irrespective of allogeneic disparity between responders and MSCs. Transwell assays revealed that the suppressive effect was primarily mediated by soluble factors that induced apoptosis. Splenocytes stimulated with alloantigen in the presence of the MSC culture supernatant (CS) produced a significant amount of IL-10, which was attributed to an increase in the number of IL-10 secreting cells, confirmed by an ELISPOT assay. The blockade of IL-10 and IL-10 receptor interaction by anti-IL-10 or anti-IL-10-receptor antibodies abrogated the suppressive capacity of MSC CS, indicating that IL-10 plays a major role in the suppression of T cell proliferation. The addition of 1-methyl-DL-tryptophan (1-MT), an indoleamine 2,3-dioxygenase (IDO) inhibitor, also restored the proliferative capacity of T cells. In conclusion, we demonstrated that soluble mediators from culture supernatant of MSCs could suppress the proliferation of both naïve and pre-activated T cells in which IL-10 and IDO play important roles.

      • 15-deoxy- <b>Δ<sub>12,14</sub></b> -prostaglandin J <b><sub>2</sub></b> Down-Regulates Activin-Induced Activin Receptor, Smad, and Cytokines Expression via Suppression of NF- <b><i><i><i>κ</i></i></i></b> B and MAPK Signaling in HepG2 Cells

        Park, Seung-Won,Cho, Chunghee,Cho, Byung-Nam,Kim, Youngchul,Goo, Tae Won,Kim, Young Il Hindawi Publishing Corporation 2013 PPAR research Vol.2013 No.-

        <P>15-Deoxy-Δ<SUP>12,14</SUP>-prostaglandin J<SUB>2</SUB> (15d-PGJ<SUB>2</SUB>) and activin are implicated in the control of apoptosis, cell proliferation, and inflammation in cells. We examined both the mechanism by which 15d-PGJ<SUB>2</SUB> regulates the transcription of activin-induced activin receptors (ActR) and Smads in HepG2 cells and the involvement of the nuclear factor-<I><I>κ</I></I>B (NF-<I><I>κ</I></I>B) and mitogen-activated protein kinase (MAPK) pathways in this regulation. Activin A (25 ng/mL) inhibited HepG2 cell proliferation, whereas 15d-PGJ<SUB>2</SUB> (2 <I><I>μ</I></I>M and 5 <I><I>μ</I></I>M) had no effect. Activin A and 15d-PGJ<SUB>2</SUB> showed different regulatory effects on ActR and Smad expression, NF-<I><I>κ</I></I>B p65 activity and MEK/ERK phosphorylation, whereas they both decreased IL-6 production and increased IL-8 production. When co-stimulated with 15d-PGJ<SUB>2</SUB> and activin, 15d-PGJ<SUB>2</SUB> inhibited the activin-induced increases in ActR and Smad expression, and decreased activin-induced IL-6 production. However, it increased activin-induced IL-8 production. In addition, 15d-PGJ<SUB>2</SUB> inhibited activin-induced NF-<I><I>κ</I></I>B p65 activity and activin-induced MEK/ERK phosphorylation. These results suggest that 15d-PGJ<SUB>2</SUB> suppresses activin-induced ActR and Smad expression, down-regulates IL-6 production, and up-regulates IL-8 production via suppression of NF-<I><I>κ</I></I>B and MAPK signaling pathway in HepG2 cells. Regulation of ActR and Smad transcript expression and cytokine production involves NF-<I><I>κ</I></I>B and the MAPK pathway via interaction with 15d-PGJ<SUB>2</SUB>/activin/Smad signaling.</P>

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