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49篇 您的检索式:作者名="Roberts 1"
    题名 作者 年代 出处 被引量
1氯吡格雷的使用与药物洗脱支架植入后远期临床结果显示文摘背景:近来的冠状动脉内药物洗脱支架研究提示,现行的抗血小板治疗方案可能并不足以预防后期支架内血栓形成。目的:于接受药物洗脱支架(drug-eluting stents,DESs)和裸金属支架(bare-metal stents,BMSs)治疗的冠状动脉病患者中评估氯吡格雷使用与患者远期结果的关系。设计、地点及患者:于连续患者中进行观察性研究。患者于2000年1月1日至2005年7月31日在杜克心脏治疗中心(一家位于北卡罗来纳州达累姆市的三级治疗中心)接受冠状动脉内支架治疗。于6、12、24个月时进行随访,直至2006年9月7日。研究人群包括4666例最初接受BMS(n=3165)或DES(n=1501)经皮冠状动脉介入治疗的患者。对随访6和12个月没有事件(没有死亡、心肌梗死或血管重建手术)的患者进行界标分析(landmark analysis)。在这些时间点上根据支架类型以及自我报告之氯吡格雷的使用情况将患者分为4组:DES使用氯吡格雷组、DES不用氯吡格雷组、BMS使用氯吡格雷组以及BMS不用氯吡格雷组。主要观测指标:随访24个月时死亡、非致命性心肌梗死以及死亡或心肌梗死之复合终点。结果:在6个月时没有事件发生的DES组患者(637例使用、579例未使用氯吡格雷)中,氯吡格雷的使用是随访24个月校正死亡率较低(使用2.0%比未使用5.3%;差异,-3.3%;95%CI,-6.3%至-0.3%;P=0.03)以及死亡或心肌梗死发生率较低(3.1%比7.2%;差异,-4.1%;95%CI,-7.6%至-0.6%;P=0.02)的显著预测指标。然而,在BMS组患者中(417例使用、1976例未用氯吡格雷),死亡(3.7%比4.5%;差异,-0.7%;95%CI,-2.9%至1.4%;P=0.50)以及死亡或心肌梗死发生率(5.5%比6.0%;差异,-0.5%;95%CI,-3.2%至2.2%;P:0.70)没有差异。在12个月随访没有事件发生的DES组患者(252例使用、276例未用氯吡格雷)中,氯吡格雷的使用依然可以预测24个月死亡(0%比3.5%;差异,-3.5%;95%CI,-5.9%至-1.1%;P=0.004)以及死亡或心肌梗死发生率(0%比4.5%;差异,-4.5%;95%CI,-7.1%至-1.9%;P〈0.001)较低。然而,在BMS组患者中(346例使用、1644例未用氯吡格雷),在死亡(3.3%比2.7%;差异,0.6%;95%CI,1.5%至2.8%;P=0.57)以及死亡或心肌梗死(4.7%比3.6%;差异,1.0%;95%CI,-1.6%至3.6%;P=0.44)发生方面,依然没有差异。结论:在接受DES治疗的患者中,延长氯吡格雷的使用可以使死亡以及死亡或心肌梗死的发生率下降。然而,使用氯吡格雷的适宜期限只能通过大型临床随机试验确定。Eric L Eisenstein, DBA Kevin J. Anstrom, PhD David F. Kong, MD Linda K. Shaw, MS Robert H. Tuttle, MSPH Daniel B. Mark, MD, MPH Judith M. Kramer, MD, MS Robert A. Harrington, MD David B. Matchar, MD David E. Kandzari, MD 1 Eric D. Peterson, MD, MPH Kevin A. Schulman, MD Robert M. Califf, MD 李呈亿(译) David E. Kandzari, MD 2007美国医学会杂志(中文版)2007,26,3:60
2Glycosylation-independent binding to extracellular domains 11-13 of mannose-6-phosphate/insulin-like growth factor-2 receptor mediates the effects of soluble CREG on the phenotypic proliferation of vascular smooth muscle cells显示文摘Background The present study aimed to investigate the detailed mode and specific sites for their binding as well as the functional relevance of this binding in the phenotypic proliferation of vascular smooth muscle cells(SMCs). Methods CREG knocked-down SMCs were employed to evaluate the biological activity of wtCREG and mCREG.Expressions of SMC differentiation markers SM myosin heavy chain(SM-MHC),SM-actin,heavy caldesmon and myocardin were determined by Western blotting using specific antibodies. Cellular growth of SMCs was assessed by bromide dewuridine (BrdU) incorporation and cell cycle analysis on fluorescence-activated cell sorting(FACS).A solid-phase binding assay was used to study the binding of CREG to extracellular domains of M6P/IGF2R.The cellular co-localization of the two recombinant CREGs with M6P/IGF2R was detected on SMC surface by immunoprecipitation and immunofluorescence analysis.Results The molecular weight of wtCREG was around 30 kD while that of the mCREG was~25 kD.Treatment of wtCREG with PNGase F reduced its molecular weight from~30 kD to~25 kD,whereas PNGase F treatment had no effect on the molecular weight of mCREG.Both wtCREG and mCREG proteins enhanced SMC differentiation,inhibited BrdU incorporation,and arrested cell cycle progression when added to the culture medium.In CREG knocked-down SMCs,the amount of CREG detected by immunoblotting in M6P/IGF2R immunoprecipitates was significantly reduced when compared to normal cells.Both recombinant CREGs co-immunoprecipitated with M6P/IGF2R, although slightly reduced amount of the mutant CREG was detected in M6P/IGF2R immunoprecipitates.Immunostaining revealed that His-tagged CREGs co-localized with IGF2R on the cell surface in a glycosylation-independent manner.In vitro binding assay showed that CREGs bound to M6P/ IGF2R extracellular domains 7-10 and 11-13 in a glycosylation -dependent and -independent manner,respectively.Further blocking experiments using soluble M6P/IGF2R fragments and M6P/IGF2R neutralizing antibody indicated that the biological activities of recombinant CREGs in SMC growth and the up-regulation of SMC differentiation markers were all abolished by treatment with the M6P/IGF2R neutralizing antibody. However,although the growth inhibitory effect of wtCREG was nearly abolished by D7-10 or D11-13,the effect of mCREG was only reversed by Dll-13,indicating that the binding to domains 11-13 is required for CREG to modulate the proliferation of SMCs.Conclusions These data suggest that solubleCREG proteins can exert their biological function via binding to the extracellular domains 7-10 and 11-13 of cell surface M6P/IGF2R in both a glycosylation-dependent and -independent manner.LUAN Bo~1,HAN Ya-ling~1,SUN Ming-yu~1,GUO Liang~1,GUO Peng~1,TAO Jie~1,DENG Jie~1,WU Guang-zhe~1,YAN Cheng-hui~1, LI Shao-hua~2 (1.Department of Cardiology,Shenyang Northern Hospital, Shenyang,China 2.Division of Vascular Surgery,Robert Wood Johnson Medical School-UMDNJ,New Jersey,USA) 2011岭南心血管病杂志2011,17,S1:5
3Ipilimumab plus dacar- bazine for previously untreated metastatic melanoma 显示文摘Robert C Thomas L Bondarenko 1 2011N Engl J Med2011,364,26:1
4Matrix metalloproteinases in the human intervertebral disc; Role in disc degeneration andscoliosis显示文摘〔1〕 Crean JKG Roberts S Jaffrat DC 1997Spine1997,22,:1
5Targeting of human immunod- eficiency vires-infected cells by CD8 + T lymplu'ytes armed with universal T-cell receptors 显示文摘Roberts MR Qin 1 Zhang Dct al 1994Blood1994,84,9:1
6A Theory of Optimum Currency Areas 显示文摘Mundel 1 Robert A 1961American Economic Review September1961,51,4:1
7Corporate FoCUS and Stock returns显示文摘Comment Robert Jarrel 1 Gregg A 1995Journalof Financ ial Economi cs1995,37,:1
8Speech and language impairment and oromotor dyspraxia due to deletion of 7q31 that involves FOXP2显示文摘Zeesman S Nowaczyk MJ Teshima 1 Roberts W Cardy JO Brian J 0,,05:1
9Per- sonality as a Predictor of Driving Performance: An Exploratory Study 显示文摘Sberrilene Classen Austin Lee Nichols Robert Mcpeek et 8 1 2011Transportation Research2011,14,5:1
10Assessment ofclinical outcomes in acute stroketrias显示文摘Roberts L Counsel 1 C 1998Stroke1998,29,5:1
119μm raman oscillator 显示文摘Robert B S Robert T K A kilohertz repetition rate 1 1989IEEE Transactions on Quan Elec1989,25,10:1
12Broken intramedullary nails 显示文摘〔8〕 Jonathab 1 Franklin M Robert A 1988JBone Joint Surg(Am)1988,70,:1
13Parametric study of coupled wall behavior-implications for the desgin of coupling beams 显示文摘Kent A H J Dan'1 Moulton Robert L C 2004Journal of Structural Engineering2004,130,12:1
14Simulation and modera- tion of the thermal response of confined pressed explosive compositions 显示文摘Dagley 1 J Robert P P David A J 1996Combustion and Flame1996,106,4:1
15The effects of Apelin on hypothalamic-pituitary- adrenal axis neuro endocrine function are mediated through corticotrophin releasing factor-and vasopressin-dependent mechanisms 显示文摘Newson M 1 Roberts EM Pope G R et at 20091 Endocrinol2009,202,1:1
16Enophthalmos correction: Principles guiding proper treatment 显示文摘Robert M Pear 1 1998Operative Techniques in Plastic and Reconstructive Surgery1998,5,4:1
17Killing kinetics of fidaxomicin and its major metabolite, OP- 1118, against Clostridium diffcile显示文摘Babakhani 1' Gomez A Robert N 2011J Med Microbiol2011,60,8:1
18Enhanced diagnostic immunofluorescence using biopsies transported in saline显示文摘Robert M Vodegel 1 Marcelus C JM de Jong 0,,04:1
19Tetracycline antibiotics: mode of action, applications, molecular biology, and epidemiology of bacterial resistance 显示文摘Chopra 1 Roberts M 2001Microbiol Mol BiolRev2001,65,2:1
20Infusion techniques for peripheral arteri- al thrombolysis显示文摘Kessel DO Berridge DC Robert~n 1 2004Cochrane Database Syst Rev2004,,00:1
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