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Circulation 10건

  1. [해외논문]   Correction to: Worsening Renal Function in Patients With Acute Heart Failure Undergoing Aggressive Diuresis Is Not Associated With Tubular Injury  


    Circulation v.137 no.25 ,pp. e853 - e853 , 2018 , 0009-7322 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  2. [해외논문]   Autopsy as a Source of Discovery in Cardiovascular Medicine : Then and Now   SCI SCIE

    Thiene, Gaetano (Department of Medical-Diagnostic Science and Special Therapies, Cardiovascular Pathology Unit, University of Padua Medical School, Italy (G.T.) ) , Saffitz, Jeffrey E. (Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA (J.E.S.).)
    Circulation v.137 no.25 ,pp. 2683 - 2685 , 2018 , 0009-7322 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  3. [해외논문]   Autopsy 2018 : Still Necessary, Even if Occasionally Not Sufficient   SCI SCIE

    Goldman, Lee (Vagelos College of Physicians and Surgeons, Columbia University, New York, NY.)
    Circulation v.137 no.25 ,pp. 2686 - 2688 , 2018 , 0009-7322 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  4. [해외논문]   Prospective Countywide Surveillance and Autopsy Characterization of Sudden Cardiac Death : POST SCD Study   SCI SCIE

    Tseng, Zian H. (Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine (Z.H.T., J.E.O.) ) , Olgin, Jeffrey E. (Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine (Z.H.T., J.E.O.) ) , Vittinghoff, Eric (Department of Epidemiology and Biostatistics (E.V.) ) , Ursell, Philip C. (Department of Pathology (P.C.U.) ) , Kim, Anthony S. (Department of Neurology (A.S.K.) ) , Sporer, Karl (Department of Emergency Medicine (K.S., C.Y.) ) , Yeh, Clement (Department of Emergency Medicine (K.S., C.Y.) ) , Colburn, Benjamin (Department of Family Medicine, Oregon Health and Science University, Portland (B.C.) ) , Clark, Nina M. (School of Medicine (N.M.C.), University of California, San Francisco ) , Khan, Rana (Weill Cornell Medical College, New York (R.K.) ) , Hart, Amy P. (Office of the Chief Medical Examiner, City and County of San Francisco, CA (A.P.H., E.M.). ) , Moffatt, Ellen (Office of the Chief Medical Examiner, City and County of San Francisco, CA (A.P.H., E.M.).)
    Circulation v.137 no.25 ,pp. 2689 - 2700 , 2018 , 0009-7322 ,

    초록

    Background: Studies of out-of-hospital cardiac arrest and sudden cardiac death (SCD) use emergency medical services records, death certificates, or definitions that infer cause of death; thus, the true incidence of SCD is unknown. Over 90% of SCDs occur out-of-hospital; nonforensic autopsies are rarely performed, and therefore causes of death are presumed. We conducted a medical examiner–based investigation to determine the precise incidence and autopsy-defined causes of all SCDs in an entire metropolitan area. We hypothesized that postmortem investigation would identify actual sudden arrhythmic deaths among presumed SCDs. Methods: Between February 1, 2011, and March 1, 2014, we prospectively identified all incident deaths attributed to out-of-hospital cardiac arrest (emergency medical services primary impression, cardiac arrest) between 18 to 90 years of age in San Francisco County for autopsy, toxicology, and histology via medical examiner surveillance of consecutive out-of-hospital deaths, all reported by law. We obtained comprehensive records to determine whether out-of-hospital cardiac arrest deaths met World Health Organization (WHO) criteria for SCD. We reviewed death certificates filed quarterly for missed SCDs. Autopsy-defined sudden arrhythmic deaths had no extracardiac cause of death or acute heart failure. A multidisciplinary committee adjudicated final cause. Results: All 20 440 deaths were reviewed; 12 671 were unattended and reported to the medical examiner. From these, we identified 912 out-of-hospital cardiac arrest deaths; 541 (59%) met WHO SCD criteria (mean 62.8 years, 69% male) and 525 (97%) were autopsied. Eighty-nine additional WHO-defined SCDs occurred within 3 weeks of active medical care with the death certificate signed by the attending physician, ineligible for autopsy but included in the countywide WHO-defined SCD incidence of 29.6/100 000 person-years, highest in black men ( P <0.0001). Of 525 WHO-defined SCDs, 301 (57%) had no cardiac history. Leading causes of death were coronary disease (32%), occult overdose (13.5%), cardiomyopathy (10%), cardiac hypertrophy (8%), and neurological (5.5%). Autopsy-defined sudden arrhythmic deaths were 55.8% (293/525) of overall, 65% (78/120) of witnessed, and 53% (215/405) of unwitnessed WHO-defined SCDs ( P = 0.024); 286 of 293 (98%) had structural cardiac disease. Conclusions: Forty percent of deaths attributed to stated cardiac arrest were not sudden or unexpected, and nearly half of presumed SCDs were not arrhythmic. These findings have implications for the accuracy of SCDs as defined by WHO criteria or emergency medical services records in aggregate mortality data, clinical trials, and cohort studies.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  5. [해외논문]   Cardiac and Noncardiac Causes of Apparent Sudden Arrhythmic Deaths : Shadows in a Spectrum   SCI SCIE

    Myerburg, Robert J. (Division of Cardiology, University of Miami Miller School of Medicine, FL.)
    Circulation v.137 no.25 ,pp. 2701 - 2704 , 2018 , 0009-7322 ,

    초록

    Background: Studies of out-of-hospital cardiac arrest and sudden cardiac death (SCD) use emergency medical services records, death certificates, or definitions that infer cause of death; thus, the true incidence of SCD is unknown. Over 90% of SCDs occur out-of-hospital; nonforensic autopsies are rarely performed, and therefore causes of death are presumed. We conducted a medical examiner–based investigation to determine the precise incidence and autopsy-defined causes of all SCDs in an entire metropolitan area. We hypothesized that postmortem investigation would identify actual sudden arrhythmic deaths among presumed SCDs. Methods: Between February 1, 2011, and March 1, 2014, we prospectively identified all incident deaths attributed to out-of-hospital cardiac arrest (emergency medical services primary impression, cardiac arrest) between 18 to 90 years of age in San Francisco County for autopsy, toxicology, and histology via medical examiner surveillance of consecutive out-of-hospital deaths, all reported by law. We obtained comprehensive records to determine whether out-of-hospital cardiac arrest deaths met World Health Organization (WHO) criteria for SCD. We reviewed death certificates filed quarterly for missed SCDs. Autopsy-defined sudden arrhythmic deaths had no extracardiac cause of death or acute heart failure. A multidisciplinary committee adjudicated final cause. Results: All 20 440 deaths were reviewed; 12 671 were unattended and reported to the medical examiner. From these, we identified 912 out-of-hospital cardiac arrest deaths; 541 (59%) met WHO SCD criteria (mean 62.8 years, 69% male) and 525 (97%) were autopsied. Eighty-nine additional WHO-defined SCDs occurred within 3 weeks of active medical care with the death certificate signed by the attending physician, ineligible for autopsy but included in the countywide WHO-defined SCD incidence of 29.6/100 000 person-years, highest in black men ( P <0.0001). Of 525 WHO-defined SCDs, 301 (57%) had no cardiac history. Leading causes of death were coronary disease (32%), occult overdose (13.5%), cardiomyopathy (10%), cardiac hypertrophy (8%), and neurological (5.5%). Autopsy-defined sudden arrhythmic deaths were 55.8% (293/525) of overall, 65% (78/120) of witnessed, and 53% (215/405) of unwitnessed WHO-defined SCDs ( P = 0.024); 286 of 293 (98%) had structural cardiac disease. Conclusions: Forty percent of deaths attributed to stated cardiac arrest were not sudden or unexpected, and nearly half of presumed SCDs were not arrhythmic. These findings have implications for the accuracy of SCDs as defined by WHO criteria or emergency medical services records in aggregate mortality data, clinical trials, and cohort studies.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  6. [해외논문]   Importance of Variant Interpretation in Whole-Exome Molecular Autopsy : Population-Based Case Series   SCI SCIE

    Shanks, Garrett W. (Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (G.W.S., D.J.T., J.P.A., M.J.A.) ) , Tester, David J. (Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (G.W.S., D.J.T., J.P.A., M.J.A.) ) , Ackerman, Jaeger P. (Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (G.W.S., D.J.T., J.P.A., M.J.A.) ) , Simpson, Michael A. (King's College London, United Kingdom (M.A.S.) ) , Behr, Elijah R. (Molecular and Clinical Sciences Research Institute, St George's University of London, London, United Kingdom (E.R.B.) ) , White, Steven M. (Office of the Medical Examiner, County of Cook, Chicago, IL (S.M.W.) ) , Ackerman, Michael J. (Department of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory (G.W.S., D.J.T., J.P.A., M.J.A.))
    Circulation v.137 no.25 ,pp. 2705 - 2715 , 2018 , 0009-7322 ,

    초록

    Background: Potentially lethal cardiac channelopathies/cardiomyopathies may underlie a substantial portion of sudden unexplained death in the young (SUDY). The whole-exome molecular autopsy represents the latest approach to postmortem genetic testing for SUDY. However, proper variant adjudication in the setting of SUDY can be challenging. Methods: From January 2012 through December 2013, 25 consecutive cases of SUDY from 1 to 40 years of age (average age at death 27±5.7 years; 13 white, 12 black) from Cook County, Illinois, were referred after a negative (n=16) or equivocal (n=9) conventional autopsy. A whole-exome molecular autopsy with analysis of 99 sudden death-susceptibility genes was performed. The predicted pathogenicity of ultrarare, nonsynonymous variants was determined using the American College of Medical Genetics guidelines. Results: Overall, 27 ultrarare nonsynonymous variants were seen in 16/25 (64%) victims of SUDY. Among black individuals, 9/12 (75%) had an ultrarare nonsynonymous variant compared with 7/13 (54%) white individuals. Of the 27 variants, 10 were considered pathogenic or likely pathogenic in 7/25 (28%) individuals in accordance with the American College of Medical Genetics guidelines. Pathogenic/likely pathogenic variants were identified in 5/16 (31%) of autopsy-negative cases and in 2/6 (33%) victims of SUDY with equivocal findings of cardiomyopathy. Overall, 6 pathogenic/likely pathogenic variants in 4/25 (16%) cases were congruent with the phenotypic findings at autopsy and therefore considered clinically actionable. Conclusions: Whole-exome molecular autopsy with gene-specific surveillance is an effective approach for the detection of potential pathogenic variants in SUDY cases. However, systematic variant adjudication is crucial to ensure accurate and proper care for surviving family members.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  7. [해외논문]   Primary Myocardial Fibrosis as an Alternative Phenotype Pathway of Inherited Cardiac Structural Disorders   SCI SCIE

    Junttila, M. Juhani (Research Unit of Internal Medicine, University of Oulu and University Hospital of Oulu, Finland (M.J.J., L.H., K.K., H.V.H.) ) , Holmströ (Research Unit of Internal Medicine, University of Oulu and University Hospital of Oulu, Finland (M.J.J., L.H., K.K., H.V.H.) ) , m, Lauri (Laboratory of Cancer Genetics and Tumor Biology, Cancer and Translational Medicine Research Unit and Biocenter Oulu (K. Pylkäs, T.M.) ) , Pylkä (Laboratory of Cancer Genetics and Tumor Biology, Cancer and Translational Medicine Research Unit and Biocenter Oulu (K. Pylkäs, T.M.) ) , s, Katri (Research Unit of Internal Medicine, University of Oulu and University Hospital of Oulu, Finland (M.J.J., L.H., K.K., H.V.H.) ) , Mantere, Tuomo (Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Research Center Oulu (K, Porvari, M.-L.K., L.P.) ) , Kaikkonen, Kari (Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Research Center Oulu (K, Porvari, M.-L.K., L.P.) ) , Porvari, Katja (Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Rese) , Kortelainen, Marja-Leena , Pakanen, Lasse , Kerkelä , , Risto , Myerburg, Robert J. , Huikuri, Heikki V.
    Circulation v.137 no.25 ,pp. 2716 - 2726 , 2018 , 0009-7322 ,

    초록

    Background: Myocardial fibrosis is a common postmortem finding among young individuals with sudden cardiac death. Because there is no known single cause, we tested the hypothesis that some cases of myocardial fibrosis in the absence of identifiable causes (primary myocardial fibrosis [PMF]) are associated with genetic variants. Methods: Tissue was obtained at autopsy from 4031 consecutive individuals with sudden cardiac death in Northern Finland, among whom PMF was the only structural finding in 145 subjects with sudden cardiac death. We performed targeted next-generation sequencing using a panel of 174 genes associated with myocardial structure and ion channel function when autopsies did not identify a secondary basis for myocardial fibrosis. All variants with an effect on protein and with a minor allele frequency <0.01 were classified as pathogenic or variants of uncertain significance on the basis of American College of Medical Genetics consensus guidelines. Results: Among the 96 specimens with DNA passing quality control (66%), postmortem genetic tests identified 24 variants of known or uncertain significance in 26 subjects (27%). Ten were pathogenic/likely pathogenic variants in 10 subjects (10%), and 14 were variants of uncertain significance in 11 genes among 16 subjects (17%). Five variants were in genes associated with arrhythmogenic right ventricular cardiomyopathy, 6 in hypertrophic cardiomyopathy–associated genes, and 11 in dilated cardiomyopathy–associated genes; 2 were not associated with these disorders. Four unique variants of uncertain significance cosegregated among multiple unrelated subjects with PMF. No pathogenic/likely pathogenic variants were detected in ion channel–encoding genes. Conclusions: A large proportion of subjects with PMF at autopsy had variants in genes associated with arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, and hypertrophic cardiomyopathy without autopsy findings of those diseases, suggesting that PMF can be an alternative phenotypic expression of structural disease–associated genetic variants or that risk-associated fibrosis was expressing before the primary disease. These findings have clinical implications for postmortem genetic testing and family risk profiling.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  8. [해외논문]   Bringing Autopsies Into the Molecular Genetic Era   SCI SCIE

    Judge, Daniel P. (Medical University of South Carolina, Division of Cardiology, Charleston (D.P.J.) ) , Brown, Emily E. (Johns Hopkins University, Division of Cardiology, Baltimore, MD (E.E.B.).)
    Circulation v.137 no.25 ,pp. 2727 - 2729 , 2018 , 0009-7322 ,

    초록

    Background: Myocardial fibrosis is a common postmortem finding among young individuals with sudden cardiac death. Because there is no known single cause, we tested the hypothesis that some cases of myocardial fibrosis in the absence of identifiable causes (primary myocardial fibrosis [PMF]) are associated with genetic variants. Methods: Tissue was obtained at autopsy from 4031 consecutive individuals with sudden cardiac death in Northern Finland, among whom PMF was the only structural finding in 145 subjects with sudden cardiac death. We performed targeted next-generation sequencing using a panel of 174 genes associated with myocardial structure and ion channel function when autopsies did not identify a secondary basis for myocardial fibrosis. All variants with an effect on protein and with a minor allele frequency <0.01 were classified as pathogenic or variants of uncertain significance on the basis of American College of Medical Genetics consensus guidelines. Results: Among the 96 specimens with DNA passing quality control (66%), postmortem genetic tests identified 24 variants of known or uncertain significance in 26 subjects (27%). Ten were pathogenic/likely pathogenic variants in 10 subjects (10%), and 14 were variants of uncertain significance in 11 genes among 16 subjects (17%). Five variants were in genes associated with arrhythmogenic right ventricular cardiomyopathy, 6 in hypertrophic cardiomyopathy–associated genes, and 11 in dilated cardiomyopathy–associated genes; 2 were not associated with these disorders. Four unique variants of uncertain significance cosegregated among multiple unrelated subjects with PMF. No pathogenic/likely pathogenic variants were detected in ion channel–encoding genes. Conclusions: A large proportion of subjects with PMF at autopsy had variants in genes associated with arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, and hypertrophic cardiomyopathy without autopsy findings of those diseases, suggesting that PMF can be an alternative phenotypic expression of structural disease–associated genetic variants or that risk-associated fibrosis was expressing before the primary disease. These findings have clinical implications for postmortem genetic testing and family risk profiling.

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  9. [해외논문]   Cardiac Implantable Electronic Device Interrogation at Forensic Autopsy : An Underestimated Resource?   SCI SCIE

    Lacour, Philipp (Charité–Universitaetsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Cardiology (P.L., A.S.P., M.H., P.A., L.-H.B., B.P., W.H., F.B.) ) , Buschmann, Claas (Campus Virchow-Klinikum, Germany. Charité–Universitaetsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Legal Medicine and Forensic Sciences, Campus Mitte, Germany (C.B.) ) , Storm, Christian (Department of Nephrology and Intensive Care Medicine (C.S., J.N.) ) , Nee, Jens (Department of Nephrology and Intensive Care Medicine (C.S., J.N.) ) , Parwani, Abdul Shokor (Charité–Universitaetsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Cardiology (P.L., A.S.P., M.H., P.A., L.-H.B., B.P., W.H., F.B.) ) , Huemer, Martin (Charité–Universitaetsmedizin Berlin, Corporate Member of Fr) , Attanasio, Philipp , Boldt, Leif-Hendrik , Rauch, Geraldine , Kucher, Andreas , Pieske, Burkert , Haverkamp, Wilhelm , Blaschke, Florian
    Circulation v.137 no.25 ,pp. 2730 - 2740 , 2018 , 0009-7322 ,

    초록

    Background: Postmortem interrogations of cardiac implantable electronic devices (CIEDs), recommended at autopsy in suspected cases of sudden cardiac death, are rarely performed, and data on systematic postmortem CIED analysis in the forensic pathology are missing. The aim of the study was to determine whether nonselective postmortem CIED interrogations and data analysis are useful to the forensic pathologist to determine the cause, mechanism, and time of death and to detect potential CIED-related safety issues. Methods: From February 2012 to April 2017, all autopsy subjects in the department of forensic medicine at the University Hospital Charité who had a CIED underwent device removal and interrogation. Over the study period, 5368 autopsies were performed. One hundred fifty subjects had in total 151 CIEDs, including 109 pacemakers, 35 defibrillators, and 7 implantable loop recorders. Results: In 40 cases (26.7%) time of death and in 51 cases (34.0%) cause of death could not be determined by forensic autopsy. Of these, CIED interrogation facilitated the determination of time of death in 70.0% of the cases and clarified the cause of death in 60.8%. Device concerns were identified in 9 cases (6.0%), including 3 hardware, 4 programming, and 2 algorithm issues. One CIED was submitted to the manufacturer for a detailed technical analysis. Conclusions: Our data demonstrate the necessity of systematic postmortem CIED interrogation in forensic medicine to determine the cause and timing of death more accurately. In addition, CIED analysis is an important tool to detect potential CIED-related safety issues.

    원문보기

    원문보기
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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  10. [해외논문]   Proteomic Architecture of Human Coronary and Aortic Atherosclerosis   SCI SCIE

    Herrington, David M. (Section on Cardiovascular Medicine, Department of Internal Medicine (D.M.H., C.F.Z., G.S.) ) , Mao, Chunhong (Biocomplexity Institute of Virginia Tech, Virginia Tech, Blacksburg (C.M.) ) , Parker, Sarah J. (Advanced Clinical Biosystems Research Institute, Cedars-Sinai Heart Institute, and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA (S.T.P., V.V., W.R.S., J.E.V.E.) ) , Fu, Zongming (Johns Hopkins Medical Institute, Baltimore, MD (Z.F.) ) , Yu, Guoqiang (Department of Electrical and Computer Engineering, Virginia Tech, Arlington (G.Y., L.C., Y.F., Yizhi Wang, Yue Wang) ) , Chen, Lulu (Department of Electrical and Computer Engineering, Virginia Tech, Arlington (G.Y., L.C., Y.F., Yizhi Wang, Yue Wang) ) , Venkatraman, Vidya (Advanced Clinical Biosystems Research Institute, Cedars-Sinai Heart Institute, and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA (S.T.P., V.V., W.R.S., J.E.V.E.) ) , Fu, Yi (Department of Electrical and Computer Engineering, Virginia Tech, Arlington (G.Y., L.C., Y.F., Yizhi Wang, Yue Wang) ) , Wang, Yizhi (Department of Electrical and Computer Engin) , Howard, Timothy D. , Jun, Goo , Zhao, Caroline F. , Liu, Yongmei , Saylor, Georgia , Spivia, Weston R. , Athas, Grace B. , Troxclair, Dana , Hixson, James E. , Vander Heide, Richard S. , Wang, Yue , Van Eyk, Jennifer E.
    Circulation v.137 no.25 ,pp. 2741 - 2756 , 2018 , 0009-7322 ,

    초록

    Backgound: The inability to detect premature atherosclerosis significantly hinders implementation of personalized therapy to prevent coronary heart disease. A comprehensive understanding of arterial protein networks and how they change in early atherosclerosis could identify new biomarkers for disease detection and improved therapeutic targets. Methods: Here we describe the human arterial proteome and proteomic features strongly associated with early atherosclerosis based on mass spectrometry analysis of coronary artery and aortic specimens from 100 autopsied young adults (200 arterial specimens). Convex analysis of mixtures, differential dependent network modeling, and bioinformatic analyses defined the composition, network rewiring, and likely regulatory features of the protein networks associated with early atherosclerosis and how they vary across 2 anatomic distributions. Results: The data document significant differences in mitochondrial protein abundance between coronary and aortic samples (coronary>>aortic), and between atherosclerotic and normal tissues (atherosclerotic<<normal), and major alterations in tumor necrosis factor, insulin receptor, peroxisome proliferator-activated receptor-α, and peroxisome proliferator-activated receptor-γ protein networks, as well, in the setting of early disease. In addition, a subset of tissue protein biomarkers indicative of early atherosclerosis was shown to predict anatomically defined coronary atherosclerosis when measured in plasma samples in a separate clinical cohort (area under the curve=0.92 [0.83–0.96]), thereby validating the use of human tissue proteomics to discover relevant plasma biomarkers for clinical applications. In addition to the specific proteins and pathways identified here, the publicly available data resource and the analysis pipeline used illustrate a strategy for interrogating and interpreting the proteomic architecture of tissues that may be relevant for other chronic diseases characterized by multicellular tissue phenotypes. Conclusions: The human arterial proteome can be viewed as a complex network whose architectural features vary considerably as a function of anatomic location and the presence or absence of atherosclerosis. The data suggest important reductions in mitochondrial protein abundance in early atherosclerosis and also identify a subset of plasma proteins that are highly predictive of angiographically defined coronary disease.

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