RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제
      • 좁혀본 항목 보기순서

        • 원문유무
        • 원문제공처
        • 학술지명
        • 주제분류
        • 발행연도
        • 작성언어
        • 저자
          펼치기

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • LEF1-mediated MMP13 gene expression is repressed by SIRT1 in human chondrocytes

        Elayyan, Jinan,Lee, Eun-Jin,Gabay, Odile,Smith, Christopher A.,Qiq, Omar,Reich, Eli,Mobasheri, Ali,Henrotin, Yves,Kimber, Susan J.,Dvir-Ginzberg, Mona The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.7

        <P>Reduced SIRT1 activity and levels during osteoarthritis (OA) promote gradual loss of cartilage. Loss of cartilage matrix is accompanied by an increase in matrix metalloproteinase (MMP) 13, partially because of enhanced LEF1 transcriptional activity. In this study, we assessed the role of SIRT1 in LEF1-mediated MMP13 gene expression in human OA chondrocytes. Results showed that MMP13 protein levels and enzymatic activity decreased significantly during SIRT1 overexpression or activation by resveratrol. Conversely, MMP13 gene expression was reduced in chondrocytes transfected with SIRT1 siRNA or treated with nicotinamide (NAM), a sirtuin inhibitor. Chondrocytes challenged with IL-113, a cytokine involved in OA pathogenesis, enhanced LEF1 protein levels and gene expression, resulting in increased MMP13 gene expression; however, overexpression of SIRT1 during IL-113 challenge impeded LEF1 levels and MMP13 gene expression. Previous reports showed that LEF1 binds to the MMP13 promoter and transactivates its expression, but we observed that SIRT1 repressed LEF1 protein and mRNA expression, ultimately reducing LEF1 transcriptional activity, as judged by luciferase assay. Finally, mouse articular cartilage from Sirt1-/presented increased LEF1 and MMP13 protein levels, similar to human OA cartilage. Thus, demonstrating for the first time that SIRT1 represses MMP13 in human OA chondrocytes, which appears to be mediated, at least in part, through repression of the transcription factor LEF1, a known modulator of MMP13 gene expression. Elayyan, J., Lee, E.-J., Gabay, O., Smith, C. A., Qiq, O., Reich, E., Mobasheri, A., Henrotin, Y., Kimber, S. J., Dvir-Ginzberg, M. LEF1-mediated MMP13 gene expression is repressed by SIRT1 in human chondrocytes.</P>

      • Poster Session : PS 0364 ; Epidemiology and Public Health : Association of Nonattendance and Emergency Assessments, Emergency Hospitalization and Mortality

        ( Diego Hernan Giunta ),( Analia Judith Baum ),( Bruno Rafael Boietti ),( Nora Angelicafuentes ),( Carolina Gabay ),( Fernan Gonzalez Bernaldo De Quiros ),( Maria Florencia Grande Ratti ),( Daniel Rob 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Introduction: Nonattendance to scheduled outpatient appointments (SOA) produces ineffi ciency and discontinuity in care, although associated impact on mortality is unknown. Objetive: Evaluate association between SOA in primary care with emergency assessments (EA), emergency hospitalization (EH) and mortality (M) throughout a year. Methods: Retrospective cohort of adults affi liated to Hospital Italiano, with at least one SOA during 2012. We included all patients beginning from the last SOA of 2012 and followed them throughout a year, describing the events of EA, EH and M. We measured the number of SOA and the nonattendance proportion at the previous year before inclusion to the cohort. We used a Cox proportional hazards regression model, to estimate crude and adjusted Hazard Ratios (HR) and 95% confi dence interval. Results: 117327 patients were included, with a median age of 59 years (IQR:34), with a female frequency of 63. 3% (74300). Median of SOA was 8 appointments (IQR 9), the median of the nonattendance proportion of each patient was 28. 6% (IQR 39). 26% of patients had a proportion of nonattendance of 50% or more. EA was 13. 5% (15858); EH was of 3% (3551); and mortality was 1. 6% (1853) during follow up. Crude HR for each 10% increase in nonattendance proportion was 1. 031 (95%, IC:1. 025- 1. 037, p<0, 001) for EA; 1, 012 (95%, IC:1-1. 025, p=0. 051) for EH; and 1. 028 (95%, IC:1. 011-1, 045, p<0, 001) for M. Adjusted HR (by sex, age, diabetes, hypertension, cancer and coronary disease) for each 10% increment in nonattendance proportion was 1. 010 (95%, IC:1. 004-1. 017, p<0, 001);1. 099 (95%, IC:1. 084-1. 113, p<0, 001); and 1. 125 (IC95% 1, 105-1, 145, p<0, 001) for EA, EF and M respectively. Conclusions: Even though the nonattendance proportion effect on EA, EH and M is moderate, it could be relevant as a prognostic factor in high risk patients subgroups.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼