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| 1 | GRADE指南:Ⅴ.证据质量评价--发表偏倚显示文摘GRADE方法中,随机试验起评即为高质量证据,观察性研究起评即为低质量证据;但若证据本身存在高发表偏倚风险,则两者证据质量级别都应降低。即使最佳证据汇总表纳入的各项研究仅有低发表偏倚风险,发表偏倚仍会极大高估效应值。当可得证据来自小样本研究、且多数由厂商资助时,作者应怀疑存在发表偏倚。若干基于检验数据类型的方法可用于评价发表偏倚,其中最常用的为漏斗图,但这些方法都有较大局限。发表偏倚可能较常见,必须特别关注早期结果、对样本量与事件数都很小的早期试验结果尤需小心。 | Gordon H.Guyatt Andrew D.Oxman Victor Montori Gunn Vist Regina Kunz Jan Brozek Pablo Alonso-Coello Ben Djulbegovic David Atkins Yngve Falck-Ytter John W.Williams Jr. Joerg Meerpohl Susan L.Norris Elie A.Akl Holger J.Schünemann 代表GRADE工作组 李幼平 王莉 钟大可 蒋兰慧 | 2011 | 中国循证医学杂志2011，11，12： | 71 |
| 2 | GRADE指南:Ⅳ.证据质量分级--研究的局限性(偏倚风险)显示文摘在GRADE方法中,若多数相关证据来自高偏倚风险的研究,则起初被定为高质量证据的随机试验和低质量证据的观察性研究均有可能被降低质量等级。随机试验已确定的局限性包括:未进行分配隐藏、未实施盲法、未报告失访情况及未恰当考虑意向性治疗原则。最近提出的局限性包括:因明显获益而早期终止试验和基于结果选择性报告结局。观察性研究的主要局限性包括使用不合适的对照及未能充分调整预后的不平衡。偏倚风险可因不同结果而异(如全死因死亡率的失访远少于生命质量的失访),许多系统评价都容易忽略这一点。在决定是否因偏倚风险而降低质量等级时,不管是随机试验还是观察性研究,作者不应采用对各个研究取平均值的方法。相反,对任何单个结果,当同时存在高、低偏倚风险的研究时,则应考虑只纳入较低偏倚风险的研究。 | Gordon H.Guyatt Andrew D.Oxman Gunn Vist Regina Kunz Jan Brozek Pablo Alonso-Coello Victor Montori Elie A.Akl Ben Djulbegovic Yngve Falck-Ytter Susan L.Norris John W.Williams Jr. David Atkins Joerg Meerpohl Holger J.Schünemann GRADE工作组 李幼平 杨晓妍 李鸿浩 李玲 | 2011 | 中国循证医学杂志2011，11，4： | 58 |
| 3 | GRADE指南:Ⅵ.证据质量评价--不精确性(随机误差)显示文摘GRADE建议通过检查95%可信区间(CI)为决定不精确性的最佳方法。在指南实际运用中,如果CI的上、下限值代表了真实效应,而临床实际情况与之不符时,必须降低证据质量级别(即对效应估计值的把握度)。除外当效应值很大且可信区间提示效应稳健,而总样本量不大且事件数很少的情况,其他应考虑因不精确性而降低证据质量级别。作此决定时,可计算有足够检验效能的单个试验所需的病例数(定义为'最优信息样本量',即optimal information size,OIS)。对连续型变量,我们建议用类似方法,首先考虑可信区间上、下限值,再计算OIS。系统评价(SR)所需方法略有不同。如果95%CI不包括相对危险度(RR)为1,且总事件发生数或病例数超过OIS标准,则精确性良好。如果95%CI包括了明显获益或危害(我们建议以RR值<0.75或>1.25作粗标准),即使达到OIS要求,因不精确性而降低证据质量级别较恰当。 | Gordon Guyatt Andrew D.Oxman Regina Kunz Jan Brozek Pablo Alonso-Coello David Rind PJ Devereaux Victor M.Montori Bo Freyschuss Gunn Vist Roman Jaeschke John W.Williams Jr. Mohammad Hassan Murad David Sinclairk Yngve Falck-Ytter Joerg Meerpohl Craig Whittington Kristian orlund Je Andrews Holger J.Schünemann 代表GRADE工作组 李幼平 王莉 陈尹 高霑 | 2011 | 中国循证医学杂志2011，11，12： | 43 |
| 4 | 肌萎缩性侧索硬化蛋白激活小胶质细胞NLRP3炎性小体显示文摘小胶质细胞NLRP3炎性小体激活正在成为神经退行性变过程中神经炎症的关键因素。诸如β-淀粉样蛋白和α-突触核蛋白之类的致病性蛋白质聚集体触发小胶质NLRP3激活,从而导致半胱天冬酶-1激活和IL-1β的分泌。在小鼠肌萎缩性侧索硬化症(ALS)的SOD1G93A模型中,半胱天冬酶-1和IL-1β均促进疾病进展,提示小胶质NLRP3在该进程中发挥作用。然而先前的研究表明,SOD1G93A小鼠小胶质细胞不表达NLRP3,SOD1G93A蛋白在小胶质细胞中产生独立于NLRP3的IL-1β。本研究论证了使用Nlrp3-GFP基因敲入小鼠,在SOD1G93A小鼠中小胶质细胞表达NLRP3。本研究显示聚集和可溶性SOD1G93A均可激活小鼠原代小胶质细胞中的炎性小体,导致半胱天冬酶-1和IL-1β裂解,ASC斑点形成以及呈剂量和时间依赖性的IL-1β分泌。重要的是,SOD1G93A无法从缺乏Nlrp3的小胶质细胞或者用特异性NLRP3抑制剂MCC950预处理的小胶质细胞中诱导IL-1β分泌,从而证实NLRP3是介导SOD1诱导的小胶质细胞IL-1β分泌的关键炎症小体复合物。在TDP-43Q331K ALS小鼠模型中也观察到小胶质NLRP3上调,TDP-43野生型和突变蛋白亦可以NLRP3依赖性的方式激活小胶质炎性小体。从机制上讲,本研究确定了活性氧簇和ATP的生成是SOD1G93A介导的NLRP3激活所需的关键事件。总之,本研究的数据表明ALS小胶质细胞表达NLRP3,而病理ALS蛋白激活小胶质NLRP3炎性小体。因此,NLRP3抑制可能是阻止小胶质细胞神经炎症和ALS疾病进展的潜在治疗方法。 | Vandana Deora John D Lee Eduardo AAlbornoz Luke McAlary Cyril J Jagaraj Avril A B Robertson Julie D Atkin Matthew A Cooper Kate Schroder Justin J Yerbury Richard Gordon Trent MWoodruff 杜一星(编译) | 2020 | 神经损伤与功能重建2020，15，9： | 13 |
| 5 | 诊断性试验和策略的证据质量和推荐强度的分级显示文摘GRADE系统能对诊断性试验或策略的证据质量和推荐强度进行分级。本文旨在阐释在此过程中如何考虑患者的重要结局, | Holger J Schünemann Andrew D Oxman Jan Brozek Paul Glasziou Roman Jaeschke Gunn E Vist John W Williams Jr Regina Kunz Jonathan Craig Victor M Montori Patrick Bossuyt Gordon H Guyatt 李晓 黄程 陈耀龙 李幼平 | 2009 | 中国循证医学杂志2009，9，5： | 7 |
| 6 | Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement显示文摘 | Scott M. Grundy James I. Cleeman Stephen R. Daniels Karen A. Donato Robert H. Eckel Barry A. Franklin David J. Gordon Ronald M. Krauss Peter J. Savage Sidney C. Smith John A. Spertus Fernando Costa | 2005 | Circulation2005，，17： | 7 |
| 7 | 代谢综合征的诊断和治疗——美国心脏协会/国立心肺血液研究所指南概要显示文摘 | Scott M. Grundy James I. Cleeman Stephen R. Daniels Karen A. Donato Robert H. Eckel Barry A.Franklin David J. Gordon Ronald M. Krauss Peter J. Savage Sidney C. Smith John A. Spertus Fernando Costa | 2006 | 世界核心医学期刊文摘(心脏病学分册)2006，2，4： | 5 |
| 8 | Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial显示文摘 | Michael P Manns John G McHutchison Stuart C Gordon Vinod K Rustgi Mitchell Shiffman Robert Reindollar Zachary D Goodman Kenneth Koury Mei-Hsiu Ling Janice K Albrecht | 2001 | The Lancet2001，，9286： | 4 |
| 9 | Characteristics, development and utilization of geothermal resources- a Nordic perspective显示文摘 | John W. Lund Leif Bjelm Gordon Bloomquist Anette K. Mortensen | 2008 | Episodes2008，31，1： | 4 |
| 10 | Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial显示文摘 | Michael P Manns John G McHutchison Stuart C Gordon Vinod K Rustgi Mitchell Shiffman Robert Reindollar Zachary D Goodman Kenneth Koury Mei-Hsiu Ling Janice K Albrecht | 2001 | The Lancet . 2001 (9286)2001，，9286： | 4 |
| 11 | Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial显示文摘 | Michael P Manns John G McHutchison Stuart C Gordon Vinod K Rustgi Mitchell Shiffman Robert Reindollar Zachary D Goodman Kenneth Koury Mei-Hsiu Ling Janice K Albrecht | 2001 | 2001 (9286)2001，，9286： | 4 |
| 12 | Efficacy of boceprevir, an NS3 protease inhibitor, in combination with peginterferon alfa-2b and ribavirin in treatment-naive patients with genotype 1 hepatitis C infection (SPRINT-1): an open-label, randomised, multicentre phase 2 trial显示文摘 | Paul Y Kwo Eric J Lawitz Jonathan McCone Eugene R Schiff John M Vierling David Pound Mitchell N Davis Joseph S Galati Stuart C Gordon Natarajan Ravendhran Lorenzo Rossaro Frank H Anderson Ira M Jacobson Raymond Rubin Kenneth Koury Lisa D Pedicone Clifford | 2010 | The Lancet2010，，9742： | 3 |
| 13 | Cytotoxic effect of interleukin-8 in retinal ganglion cells and its possible mechanisms显示文摘AIM: To investigate the effect of interleukin-8(IL-8) on neural retinal ganglion cells(RGCs) and whether it can be alleviated by G31P. METHODS: RGC-5 cells were exposed to IL-8 with or without its specific receptor antagonist G31P for 24h, and the cell viability was assessed by Cell Counting Kit 8(CCK-8). Apoptosis was measured by examining nuclear morphology and quantifying with flow cytometry. Reverse transcription quantitative real-time polymerase chain reaction(RT-qP CR) and Western blot were used to investigate the expression of apoptosis-related genes. RESULTS: CCK-8 assay showed that IL-8 significantly inhibits the viability of RGC-5 cells in a dose-dependent manner. Cell apoptosis assays exhibited higher apoptotic rate in IL-8 treatment group compared to control group. We further found that IL-8 could promote Bax and caspase-3 expressions, but decrease the level of Bcl-2 in the aspect of m RNA and protein. However, pre-treatment with G31P partly attenuated these effects in RGC-5 cells(P<0.05).CONCLUSION: These results indicate that anti-proliferation effects of IL-8 through induction of cell apoptosis regulated by Bcl-2, Bax and caspase-3 expressions, can be ameliorated by G31P. | Jing-Jing Wang Walana Williams Bing Wang Jing Wei Xia Lu Jya-Wei Cheng John R Gordon Jing-Min Li Fang Li | 2018 | International Journal of Ophthalmology(English edition)2018，11，8： | 3 |
| 14 | Sofosbuvir and Ribavirin Prevent Recurrence of HCV Infection after Liver Transplantation: An Open-Label Study显示文摘 | Michael P. Curry Xavier Forns Raymond T. Chung Norah A. Terrault Robert Brown Jonathan M. Fenkel Fredric Gordon Jacqueline O’Leary Alexander Kuo Thomas Schiano Gregory Everson Eugene Schiff Alex Befeler Edward Gane Sammy Saab John G. McHutchison G. Mani S | 2014 | Gastroenterology2014，，： | 3 |
| 15 | Increased catabolism and decreased unsaturation of ganglioside in patients with inflammatory bowel disease显示文摘AIM: To investigate whether accelerated catabolism of ganglioside and decreased ganglioside content contribute to the etiology of pro-inflammatory intestinal disease. METHODS: Intestinal mucosa from terminal ileum or colon was obtained from patients with ulcerative colitis or inflammatory Crohn's disease(n = 11) undergoing bowel resection and compared to control samples of normal intestine from patients with benign colon polyps(n = 6) and colorectal cancer(n = 12) in this observational case-control study. Gangliosides and phospholipids of intestinal mucosa were characterized by class and ceramide or fatty acid composition using liquid chromatography triple-quad mass spectrometry. Content and composition of ganglioside classes GM1, GM3, GD3, GD1 a, GT1 and GT3 were compared among subject groups. Content and composition of phospholipid classes phosphatidylcholine(PC) and phosphatidylethanolamine were compared among subject groups. Unsaturation index of individual ganglioside and phospholipid classes was computed and compared among subject groups. Ganglioside catabolism enzymes beta-hexosaminidase A(HEXA) and sialidase-3(NEU3) were measured in intestinal mucosa using western blot and compared among subject groups. RESULTS: Relative GM3 ganglioside content was 2-fold higher(P < 0.05) in intestine from patients with inflammatory bowel disease(IBD) compared to control intestine. The quantity of GM3 and ratio of GM3/GD3 was also higher in IBD intestine than control tissue(P < 0.05). Control intestine exhibited 3-fold higher(P < 0.01) relative GD1 a ganglioside content than IBD intestine. GD3 and GD1 a species of ganglioside containing three unsaturated bonds were present in control intestine, but were not detected in IBD intestine. The relative content of PC containing more than two unsaturated bonds was 30% lower in IBD intestine than control intestine(P < 0.05). The relative content of HEXA in IBD intestine was increased 1.7-fold(P < 0.05) and NEU3 was increased 8.3-fold(P < 0.01) compared to normal intestine. Intestinal mucosa in IBD is characterized by increased GM3 content, decreased GD1 a, and a reduction in polyunsaturated fatty acid constituents in GD3, GD1 a and PC.CONCLUSION: This study suggests a new paradigm by proposing that IBD occurs as a consequence of increased metabolism of specific gangliosides. | John J Miklavcic Glen K Shoemaker Vera C Mazurak M Tom Clandinin Tasha DL Hart Kareena L Schnabl Gordon M Lees Bodil MK Larsen Oliver F Bathe Alan BR Thomson M Tom Clandinin | 2015 | World Journal of Gastroenterology2015，21，35： | 3 |
| 16 | NLRP6 Inflammasome Regulates Colonic Microbial Ecology and Risk for Colitis显示文摘 | Eran Elinav Till Strowig Andrew L. Kau Jorge Henao-Mejia Christoph A. Thaiss Carmen J. Booth David R. Peaper John Bertin Stephanie C. Eisenbarth Jeffrey I. Gordon Richard A. Flavell | 2011 | Cell2011，，5： | 3 |
| 17 | Sofosbuvir with pegylated interferon alfa-2a and ribavirin for treatment-naive patients with hepatitis C genotype-1 infection (ATOMIC): an open-label, randomised, multicentre phase 2 trial显示文摘 | Kris V Kowdley Eric Lawitz Israel Crespo Tarek Hassanein Mitchell N Davis Michael DeMicco David E Bernstein Nezam Afdhal John M Vierling Stuart C Gordon Jane K Anderson Robert H Hyland Hadas Dvory-Sobol Di An Robert G Hindes Efsevia Albanis William T Symo | 2013 | The Lancet2013，，9883： | 3 |
| 18 | SJES14110700383743显示文摘 | Peter J. Murray Judith E. Allen Subhra K. Biswas Edward A. Fisher Derek W. Gilroy Sergij Goerdt Siamon Gordon John A. Hamilton Lionel B. Ivashkiv Toby Lawrence Massimo Locati Alberto Mantovani Fernando O. Martinez Jean-Louis Mege David M. Mosser Gioacchin | 2014 | Immunity2014，，1： | 2 |
| 19 | Phlegmonous gastritis: case report and review显示文摘 | Gordon Y. Kim John Ward Bruce Henessey Joyce Peji Christopher Godell Hiwot Desta Scott Arlin John Tzagournis Fred Thomas | 2005 | Gastrointestinal Endoscopy2005，，1： | 2 |
| 20 | Label-retaining liver cancer cells are relatively resistant to sorafenib显示文摘 | Hong-Wu Xin Chenwi M Ambe Danielle M Hari Gordon W Wiegand Tyler C Miller Jin-Qiu Chen Andrew J Anderson Satyajit Ray John E Mullinax Tomotake Koizumi Russell C Langan Douglas Burka Michelle A Herrmann Paul K Goldsmith Alexander Stojadinovic Udo Rudloff S | 2013 | Gut2013，，12： | 2 |
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