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( Dong Hyuk Sheen ),( Seung Jae Hong ),( Sang Heon Lee ),( Hye Soon Lee ),( Won Tae Chung ),( Hongsi Jiang ),( Sungmin Lee ),( Dae Hyun Yoo ) 대한류마티스학회 2019 대한류마티스학회지 Vol.26 No.1
Objective. Evaluate effectiveness/safety of tacrolimus in patients in Korea with active rheumatoid arthritis (RA) and unsuccessful response to disease-modifying anti-rheumatic drugs (DMARDs). Methods. Open-label, single-arm, non-comparative, 24-week, Phase-IV study in patients with active RA who had taken DMARDs for >6 months. Following a washout period, tacrolimus was initiated (baseline-12 weeks; dose 2 mg/day and 1.5 mg/day in patients aged ≤65 and >65 years, respectively). After 12 weeks, dose could be adjusted (remaining between 1~3 mg); treatment continued to 24 weeks. Primary endpoint was American College of Rheumatology 20% improvement (ACR20) (baseline-Week 24). Secondary endpoints included ACR50/ACR70 response, disease-activity score in 28 joints (DAS28) erythrocyte sedimentation rate (ESR), number of tender/ swollen joints, and bone mineral density (BMD) loss. Adverse events (AEs) were recorded. Results. Overall, 121 patients were analysed. Mean ±standard deviation tacrolimus dose baseline-Week 24 was 1.81±0.47 mg/day. After 24 weeks, 64.5%, 39.7%, and 19.0% of patients were ACR20, ACR50, and ACR70 responders, respectively. DAS28-ESR score decreased from 5.5±0.8 (baseline) to 3.7±1.5 (Week 24; p<0.0001); number of tender/swollen joints decreased. Between screening and Week 24, change in BMD-T score in lumbar and femur regions was -0.06±0.38 (p=0.1550) and -0.04±0.28 (p=0.0936), respectively, with no significant change in International Society for Clinical Densitometry classification. Fifty-six (46.3%) patients experienced 93 AEs; 75.3% were mild. No unexpected safety signals identified. Conclusion. Tacrolimus therapy was associated with a high proportion of ACR responders, and improved DAS28-ESR score and physical joint function during the study. Tacrolimus may be a suitable therapy for DMARD-resistant patients with RA. (J Rheum Dis 2019;26:20-30)
박효 ( Hyo Park ),신동혁 ( Dong Hyuk Sheen ),임미경 ( Mi Kyoung Lim ),심승철 ( Seung Cheol Shim ) 대한류마티스학회 2012 대한류마티스학회지 Vol.19 No.4
Systemic lupus erythematosus (SLE) is an autoimmune disorder affected by multiple genetic, hormonal and environmental factors, which makes it impossible to identify the exact cause of this ailment by only investigating SLE patients, who are genetically heterogeneous, and live in various environments. Therefore, the study of mouse models of lupus has provided valuable clues to help identify, and to validate, novel molecular pathways and targets implicated in the pathogenesis of the disease. While there is no perfect model to reflect all the disease phenotypes observed in human patients, disease subsets are represented in various animal models, which allows modulation of a particular pathophysiological pathway, resulting in the possibility of dissecting its specific contribution to disease development. Spontaneous mouse models of lupus have led to identification of numerous susceptibility loci, from which several candidate genes have been found, while induced models of lupus have provided insight into the role of environmental factors, as well as a better understanding of the cellular mechanisms by which SLE develops. Animal models also allow us to screen and evaluate potential preventive and therapeutic agents. Correlation of specific pathways in animal models to subsets of human disease offers the unique possibility of more accurate preclinical predictions of efficacy for single or combinatorial therapeutic approaches in the clinic. Here, we introduce various animal models of SLE, and review current data focused on genetic factors that are associated with susceptibility or phenotypes of lupus, leading into the present understanding of the genetic basis in lupus pathogenesis.
박효 ( Hyo Park ),신동혁 ( Dong Hyuk Sheen ),임미경 ( Mi Kyoung Lim ),심승철 ( Seung Cheol Shim ) 대한류마티스학회 2014 대한류마티스학회지 Vol.21 No.6
본 논문의 Table 5의 내용과 타국제학술지의 Table 내용의 동일함이 확인되어 편집위원회 회의결과 해당논문을 게재철회 하기로 결정하였습니다. http://dx.doi.org/10.4078/jrd.2012.19.4.173
Lim, Mi-Kyoung,Sheen, Dong-Hyuk,Lee, Yun Jung,Mun, You Ri,Park, Mira,Shim, Seung-Cheol Journal of Rheumatology Pub. Co 2009 The Journal of rheumatology Vol.36 No.4
<P>OBJECTIVE: To determine whether anti-cyclic citrullinated peptide (anti-CCP) antibodies, which are a highly specific test for rheumatoid arthritis (RA), could differentiate between hepatitis B virus (HBV)-associated arthropathy and concomitant RA in Korean patients with chronic HBV infection. METHODS: We investigated 240 patients with HBV infection. Anti-CCP antibodies were measured by ELISA and rheumatoid factor (RF) by the latex fixation test. Patient records were reviewed, and a standard form was used to record all demographic, clinical, and laboratory characteristics. Patients were divided into 4 groups according to joint symptoms: asymptomatic, arthralgia, oligoarthritis, and RA. We categorized liver disease into 3 groups: carrier, chronic hepatitis, and cirrhosis. RESULTS: Anti-CCP antibodies and RF were detected in 11 and 28 of 240 patients, respectively. Anti-CCP antibodies were detected in 9 of 10 RA (90%) and 2 of 230 non-RA patients (0.86%). The positive rate for RF was 90% in RA and 8.3% in non-RA. Eight of 10 RA patients were positive for both RF and anti-CCP antibodies. RF was detected in 11 patients without joint symptoms, 4 with arthralgia, and 4 with oligoarthritis, whereas anti-CCP antibodies were found in 1 patient without joint symptoms and 1 with oligoarthritis. Specificity of anti-CCP antibody for RA was 99.1%, whereas RF showed 91.7% specificity (p<0.0002). We compared the titers and positive detection rates of anti-CCP antibodies and RF among liver disease subgroups. There was no significant between-subgroup difference. CONCLUSION: Measurement of anti-CCP antibodies is better than RF detection to discriminate HBV-associated arthropathy from concomitant RA in patients with chronic HBV infection.</P>
Kim, Ji-Young,Lim, Mi-Kyoung,Sheen, Dong-Hyuk,Kim, Chan,Lee, So-Young,Park, Hyo,Lee, Min-Ji,Lee, Sang-Kwang,Yang, Yun-Sik,Shim, Seung-Cheol The Korean Association of Immunobiologists 2011 Immune Network Vol.11 No.5
Background: Current management strategies attempt to diagnose rheumatoid arthritis (RA) at an early stage. Transcription profiling is applied in the search for biomarkers for detecting early-stage disease. Even though gene profiling has been reported using several animal models of RA, most studies were performed after the development of active arthritis, and conducted only on the peripheral blood and joint. Therefore, we investigated gene expression during the initial phase of collagen-induced arthritis (CIA) before the arthritic features developed in the thymus in addition to the peripheral blood and synovium. Methods: For gene expression analysis using cDNA microarray technology, samples of thymus, blood, and synovium were collected from CIA, rats immunized only with type II collagen (Cll), rats immunized only with adjuvant, and unimmunized rats on days 4 and 9 after the first immunization. Arrays were scanned with an Illumina bead array. Results: Of the 21,910 genes in the array, 1,243 genes were differentially expressed at least 2-fold change in various organs of CIA compared to controls. Among the 1,243 genes, 8 encode T-cell receptors (TCRs), including CD3${\zeta}$, CD3${\delta}$, CD3${\varepsilon}$, CD8${\alpha}$, and CD8${\beta}$ genes, which were down-regulated in CIA. The synovium was the organ in which the genes were differentially expressed between CIA and control group, and no difference were found in the thymus and blood. Further, we determined that the differential expression was affected by adjuvant more than Cll. The differential expression of genes as revealed by real-time RT-PCR, was in agreement with the microarray data. Conclusion: This study provides evidence that the genes encoding TCRs including CD3${\zeta}$, CD3${\delta}$, CD3${\varepsilon}$, CD8${\alpha}$, and CD8${\beta}$ genes were down-regulated during the initial phase of CIA in the synovium of CIA. In addition, adjuvant played a greater role in the down-regulation of the CD3 complex compared to CII. Therefore, the down-regulation of TCR gene expression occurred dominantly by adjuvant could be involved in the pathogenesis of the early stage at CIA.
Chan Kim,Toyou Kim,Jihyung Yoo,Dong-Hyuk Sheen,Sang Kwang Lee,Eun-Hye Choi,Tong Jin Chun,Seong-wook Kang,Seung-Cheol Shim,Mi-Kyoung Lim 질병관리본부 2017 Osong Public Health and Research Persptectives Vol.8 No.3
Objectives: The objectives of this study were to evaluate the long-term effect of anti-platelet treatment on the radiological progression of collagen-induced arthritis in rats. Methods: Female Lewis rats with collagen-induced arthritis were divided into three experimental groups: saline, aspirin monotherapy (n = 12), and aspirin–clopidogrel dual therapy (n = 12). Drugs were administered daily and continued up to 70 days after the induction of arthritis. The clinical arthritis index (weight, morphology score, and paw thickness) and radiological scores were evaluated. Results: The clinical arthritis index peaked on day 20, while the radiological scores peaked on day 35. No intergroup difference was observed in the clinical arthritis index throughout the experiment. The aspirin–clopidogrel dual therapy group had a significantly higher mean radiological score than the other groups (p = 0.045) on day 35. Further treatments resulted in significantly improved radiological findings in the aspirin monotherapy and aspirin–clopidogrel dual therapy groups on day 70 but no significant improvement in the saline group. Conclusion: Anti-platelet agent treatment improved radiological findings on day 70. These observations emphasize the importance of a future long-term study of the effects of anti-platelet agent treatment on arthritis.
허민영 ( Min Young Her ),신동혁 ( Dong Hyuk Sheen ),김태환 ( Tae Hwan Kim ) 대한류마티스학회 2006 대한류마티스학회지 Vol.13 No.1
The conventional approach to treatment of patients with ankylosing spondylitis (AS) have been rather limited in the last decades. Evidence is accumulating that tumor necrosis factor (TNF) blocker is highly effective in AS. This article reviews the most recent and the most pertinent advances in the treatment in AS. TNF blocker have been evaluated in a number of randomized controlled trials in AS and have been demonstrated to be effective in disease activity, function, and quality of life in these patients. TNF blocker is emerging as the best therapeutic option available for patients with AS.
김성수,Pil-Jae Kong,김봉석,Dong-Hyuk Sheen,Su-Youn Nam,전완주 대한약학회 2004 Archives of Pharmacal Research Vol.27 No.3
Microglia are the major inflammatory cells in the central nervous system and become activated in response to brain injuries such as ischemia, trauma, and neurodegenerative diseases including Alzheimer's disease (AD). Moreover, activated microglia are known to release a variety of proinflammatory cytokines and oxidants such as nitric oxide (NO). Minocycline is a semisynthetic second-generation tetracycline that exerts anti-inflammatory effects that are completely distinct form its antimicrobial action. In this study, the inhibitory effects of minocycline on NO and prostaglandin E2 (PGE2) release was examined in lipopolysaccharides (LPS)-challenged BV2 murine microglial cells. Further, effects of minocycline on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression levels were also determined. The results showed that minocycline significantly inhibited NO and PGE2 production and iNOS and COX-2 expression in BV2 microglial cells. These findings suggest that minocycline should be evaluated as potential therapeutic agent for various pathological conditions due to the excessive activation of microglia.