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      • 증예(症例) : Type 2 Arnold Chiari Malformation의 산전진단 1예

        류완희 ( Wan Hee Yoo ),정민 ( Min Jeong ),정영주 ( Young Ju Jeong ),김관식 ( Kwan Sik Kim ),박종관 ( Jong Kwan Park ),조성남 ( Sung Nam Cho ) 전북대학교 의과학연구소 2003 全北醫大論文集 Vol.27 No.2

        Arnold-Chiari II형 기형은 뇌실확장증을 일으킬 수 있는 기형 증의 하나이며 대부분 예후가 불량하므로 산전 초음파상 뇌실확장증이 발견되면 반드시 후두와(posterior fossa)의 검사와 척추에 대한 정밀검사가 시행되어야 할 것으로 사료된다. 본원에서 뇌실확장증이 발견되어 전원된 환자에서 정밀 초음파를 통해 Arnold-Chiari II형 기형을 진단한 1예를 경험하였기에 간단한 문헌고찰과 함께 보고하는 바이다. Arnold-Chiari malformation is a complex abnormality, consisting of various combinations of brainstem and cerebellar malformations, usually associated with ventriculomegaly and spinal defects. A 29-year-old pregnant woman at 28 weeks gestation was refered after detection of ventriculomegaly. We also found myelomeningocele and indirect cranial markers: the lemon sign, the banana sign, ventriculomegaly. and then we decided this finding was Arnold Chiari II malformation. We present this cases with a brief review of literatures.

      • SCOPUSKCI등재
      • KCI등재

        전신홍반루푸스 환자에서 IFN-α에 의한 CD4+ T 림프구의 ERK Phosphorylation의 감소

        류완희 ( Wan Hee Yoo ) 대한류마티스학회 2006 대한류마티스학회지 Vol.13 No.3

        Objective: CD4+ T cells from patients with systemic lupus erythematosus (SLE) display aberrant TCR signaling and IFN-α plays critical roles in the pathogenesis of SLE; however, the effects of IFN-α on disease-associated TCR signaling defects remain unknown. This study investigated the ERK phosphorylation during TCR triggering and the effects of IFN-α on ERK signaling in CD4+ T cells. Methods: CD4+ T lymphocytes were sorted from PBMC using magnetic beads in patients with SLE who met the 1982 revised ACR criteria for SLE and age-matched healthy controls. The phosphorylation of ERK 1/2 was analyzed by flow cytometry and mean fluorescent intensity was measured to define the degree of phosphorylation of ERK. In some experiments, anti-CD3 stimulation was performed after preincubation with patient or control serum, diluted in tissue culture media, with or without addition of an anti-IFN-α antibody. The serum level of IFN-α was measured by ELISA. Results: ERK-1/2 phosphorylation was decreased in CD4+ T cells of lupus patients than healthy controls and associated with disease activity. Pre-incubation of control CD4+ T cells with allogeneic lupus plasma decreased ERK-1/2 phosphorylation more than allogeneic control and RA plasma and this was reversed by anti-IFN-α Ab. Accordingly, ERK-1/2 phosphorylation was decreased in control CD4+ T cells pre-incubation with lupus plasma with high IFN-α levels more than lupus plasma with non-detectable IFN-α levels. Recombinant IFN-α inhibited TCR-mediated ERK-1/2 phosphorylation dose-dependently. Conclusion: These results suggest that IFN-α stimulation in vivo may underlie the aberrant TCR-mediated MAPK signaling in lupus CD4+ T cells and associated with disease pathogenesis.

      • SCOPUSKCI등재

        저산소증에 의한 활막 섬유모세포의 ICAM-1 발현에 대한 항산화제의 영향

        김정렬,류완희,Kim, Jung Ryul,Yoo, Wan Hee 대한면역학회 2002 Immune Network Vol.2 No.1

        Background: Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial hyperplasia and joint destruction. The synovial fibroblasts express cell adhesion molecules and have a role in adhesive interation with inflammatory cells in synovial tissue. It has been suggested that hypoxic conditioins are thought to exist in arthritic joints, and several studies indicate that reactive oxygen species (ROS) produced in hypoxic condition can initiate events that lead to pro-adhesive changes via increased expression of adhesion molecules. So, this study wsa designed to examine whether antioxidant can inhibit hypoxia-induced expression of ICAM-1 in cultured human synovial fibroblasts. Methods: Synovial fibroblasts were isolated from synovial tissue in patients with RA and cultured at hypoxic condition. Antioxidant, PDTC (pyrrolidine dithiocarbamate) were pre-treated for an hour before the hypoxic culture and synovial fibroblasts were harvested at 0, 6, 12, 24, 48 hours time points. Cell surface ICAM-1 expression in synovial fibroblasts was examined by the flow cytometric analysis. To analyse the expression of ICAM-1 mRNA, reverse-transcriptase polymerase chain reaction (RT-PCR) was performed. The levels of cytokines in culture supernatants were measured by ELISA, and activation of NF-${\kappa}B$ was analysed by electrophoretic mobility shift assay. The adhesive reaction between synovial fibroblasts and lymphocytes was assayed by measurement of fluorescent intensity of BCECF-AM in lymphocytes. Results: Hypoxic stimuli up-regulated the ICAM-1 expression as well as the adhesive interaction of human synvial fibroblasts to lymphocytes in a time-dependent manner, and PDTC inhibited hpyoxia-induced ICAM-1 expression and cell-cell interaction. PDTC also inhibited the hypoxia-induced activation of intracellular transcription factor, NF-${\kappa}B$. PDTC decreased the amount of hypoxia-induced production of IL-$1{\beta}$ and TNF-${\alpha}$. Conclusion: These studies demonstrate that PDTC inhibit the hypoxia-induced expression of the adhesion molecule, ICAM-1 and activation of NF-${\kappa}B$ in cultured human synovial fibroblasts.

      • KCI등재

        Rhupus Syndrome 환자에서 발생한 Lupus Enteritis

        박지현 ( Ji Hyun Park ),류완희 ( Wan Hee Yoo ),박태선 ( Tae Sun Park ),백홍선 ( Hong Sun Baek ) 대한류마티스학회 1999 대한류마티스학회지 Vol.6 No.2

        Rheumatoid arthritis(RA) and systemic lupus erythematosus(SLE) are common rheumatologic diseases, and considered to be separate diseases with defined criteria for diagnosis. Occasionally, patients with overlapping features of RA and SLE, termed rhupus syndrome, have been encountered. Appreciation of these patients with rhupus is important since their therapy and outcome differ from those having RA or SLE alone. Rhupus syndrome is a systemic disease which can involve gastrointestinal tract as SLE alone. Lupus enteritis, most feared gastrointestinal complication of SLE, can develop in rhupus syndrome, Recently, we experienced a 54-year-old female patient with lupus enteritis during treatment of rhupus syndrome and present the case here with brief review of literatures.

      • KCI등재

        종설 : 류마티스 질환의 생물학적 치료제

        홍명주 ( Myong Joo Hong ),류완희 ( Wan Hee Yoo ) 대한내과학회 2012 대한내과학회지 Vol.82 No.5

        During the past three decades the treatment in rheumatology was revolutionized by the introduction of disease-modifying anti-rheumatic drugs. Advances in our understanding of the pathogenesis of rheumatic diseases have led to the discovery of critical pathogenetic mechanisms of inflammation and autoimmunity and the invention of new target-specific biologic agents. The development of biologic agents led to a new era in treatment of various rheumatic diseases. Treatments of rheumatic diseases such as rheumatoid arthritis (RA) had been very difficult in former days until conventional DMARDs was developed. Although synthetic DMARDs made it a lot easier to control rheumatic diseases, still, there were some difficulties on controlling diseases. The biologic agents inhibit specific pro-inflammatory cytokines as a targeted therapy to prevent inflammation and destruction of affected joint and/or tissues. Three TNF blocking agents, etanercept, infliximab and adalimumab, are the most well recognized and widely used biologic agents in RA, ankylosing spondylitis (AS), and some other inflammatory autoimmune diseases. Furthermore, an inhibitor of IL-1 (anakinra), a B-cell depleting drug (rituximab) and an inhibitor of T-cell costimulation (abatacept) are developed in turn asnovel biologic agents which are believed to be effective in number of rheumatic diseases. Recently, an inhibitor of IL-6 (tocilizumab) and 2 other TNF inhibitors (golimumab and certolizumab) are developed. Here, the brief descriptions of recently used biologic agents and their efficacies and safeties are discussed. (Korean J Med 2012;82:549-561)

      • KCI등재

        류마티스 관절염의 활막 섬유모세포에서 Hypoxia/reoxygenation에 의한 종양 억제 인자 PTEN 발현의 조절

        이학용 ( Hak Yong Lee ),류완희 ( Wan Hee Yoo ) 대한류마티스학회 2004 대한류마티스학회지 Vol.11 No.4

        Objective: The lack of phosphatase and tensin homolgue deleted on chromosome ten (PTEN) expression was described in rheumatoid synovial tissues and synovial fibroblasts, but exact cause of that in RA is not well known. Hypoxic conditions are thought to exist in inflamed arthritic synovium and therefore, this study was designed to investigate the effects of hypoxia/reoxygenation on the expression of PTEN in synovial fibroblasts of rheumatoid arthritis. Methods: Synovial fibroblasts were isolated from synovial tissues of patients suffering from RA and hypoxic culture was performed by incubating cells in 5% CO2 incubator held at 3% oxygen by the addition of nitrogen gas for 24 hours. Then synovial fibroblasts were cultured for 10 min under normoxic condition for reoxygenation. To know the expression of PTEN and phosphorylated Akt (p-Akt) in synovial fibroblasts, Western blotting analysis was performed. The expression of PIP3 kinase and PTEN was analyzed by immunocytochemical staining. Results: There were less PTEN expression in rheumatoid synovial fibroblasts than that of healthy controls. Hypoxic/reoxygenation stimuli induced down-regulation of PTEN expression in the rheumatoid synovial fibroblasts. In contrast, the expression of PIP3 and p-Akt was increased after stimulation with hypoxia/reoxygenation. Conclusion: These studies suggest that hypoxia/reoxygenation could cause the reduced expression of PTEN in rheumatoid synovial fibroblasts and thus it might thereby contribute to the invasive behaviour of rheumatoid synovial fibroblasts by maintaining their aggressive phenotype in RA.

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