|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | GRADE指南:Ⅰ.导论--GRADE证据概要表和结果总结表显示文摘本文是GRADE(Grading of Recommendations Assessment,Development,and Evaluation)系列文章的导论。该系列文章为使用GRADE系统提供指导,介绍如何将该系统用于系统评价、卫生技术评估(HTAs)及临床实践指南中备选方案的证据质量评价和推荐强度评级。GRADE方法始于提出一个明晰的问题,包括对所有重要结果的详细说明。证据被收集和汇总后,GRADE提供了明确的标准来评价其质量,包括研究设计、偏倚风险、不精确性、不一致性、间接性及效应量大小。根据支撑证据质量及备选方案带来的预期和非预期结果间的平衡情况,推荐强度以强/弱(或表述为'有条件的'/'任意的')作为特征。GRADE建议用简洁、透明、信息量丰富的结果总结表来汇总证据(以显示证据质量及每一重要结果的相对效应量和绝对效应量),和(或)以证据概要表形式额外提供证据质量评价理由的详细信息。本系列的后续文章涉及如何采用GRADE方法明确构建问题、评价证据质量及形成推荐意见。 | Gordon Guyatt Andrew D.Oxman Elie Akl Regina Kunz Gunn Vist Jan Brozek Susan Norris Yngve Falck-Ytter Paul Glasziou Hans deBeer Roman Jaeschke David Rind Joerg Meerpohl Philipp Dahm Holger J.Schünemann GRADE工作组 李幼平 杨晓妍 蒋兰慧 沈建通 | 2011 | 中国循证医学杂志2011，11，4： | 205 |
| 2 | 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 |
| 3 | GRADE指南:Ⅶ.证据质量评价--不一致性显示文摘本文针对二分类变量结局指标相对(而非绝对)治疗效果的不一致性。证据本身不会因不同研究结果具有一致性而升级,但可能因不一致而降低质量级别。衡量一致性的标准包括点估计值的相似性、可信区间的重叠程度以及统计学判定标准包括异质性检验和I2。系统评价作者应提出并检验少数几个与患者、干预措施、结局指标以及方法学相关的先验假设以探寻异质性来源。当不一致性很大且无法解释时,因不一致性而降低质量级别是恰当的,特别当某些研究显示有显著益处而其他显示无益甚至有害时(而非仅是疗效大与疗效小的比较)。明显的亚组效应可能不可靠。如果亚组效应满足以下条件,其可信度将会增加:基于少数几个有具体方向的先验假设、亚组比较来自研究内而非研究间、交互检验的P值小、结果有生物学意义。 | Gordon H.Guyatt Andrew D.Oxman Regina Kunz James Woodcock Jan Brozek Mark Helfand Pablo Alonso-Coello Paul Glasziou Roman Jaeschke Elie A.Akl Susan Norris Gunn Vist Philipp Dahm Vijay K.Shukla Julian Higgins Yngve Falck-Ytter Holger J.Schünemann 代表GRADE小组 李幼平 杨晓妍 王莉 蔡羽嘉 陈群飞 | 2011 | 中国循证医学杂志2011，11，12： | 33 |
| 4 | GRADE指南:Ⅷ.证据质量评价--间接性显示文摘直接证据来自直接比较我们关注的干预措施用于我们关注的患者人群,并测量患者重要结局的研究。间接证据可由以下4种方式之一产生。第一,患者可能与我们关注的患者不同(适用性一词常用于这类间接性)。第二,所检验的干预措施可能与我们关注的干预措施不同。有关患者和干预措施间接性的决策取决于对生物或社会因素差异是否大到可能使效应尺度出现预期的较大差异的考虑。第三,结果可能有别于最初设定的结局指标——如替代结果本身不重要,但测量之是基于替代结果的变化反映患者重要结局变化这一假设。第四类间接性在概念上与前三类不同,发生于临床医生必须在未经直接比较的两种干预措施间做出选择时。这种情况下比较治疗方案需要特定的统计方法,并根据患者人群、联合干预措施、结局测量指标及备选干预措施试验方法的差异程度,将证据级别降低1或2级。 | Gordon Guyatt Andrew D.Oxman Regina Kunz James Woodcock Jan Brozek Mark Helfand Pablo Alonso-Coello Yngve Falck-Ytter Roman Jaeschke Gunn Vist Elie A.Akl Piet N Post Susan Norris Joerg Meerpohl Mona Nasser 代表GRADE工作组 李幼平 杨晓妍 李鸿浩 | 2011 | 中国循证医学杂志2011，11，12： | 30 |
| 5 | 意见不一致时的策略:应用GRADE网格对临床实践指南达成共识显示文摘指南制定委员会的结构庞大和多元化使达成共识变得困难。Roman Jaeschke及其同事阐述了一种达成共识的简单方法,即当无法取得一致时,应用GRADE网格对临床实践指南达成共识。 | Roman Jaeschke Gordon H Guyatt Phil Dellinger Holger Schünemann Mitchell M Levy Regina Kunz Susan Norris Julian Bion 刘芳 陈耀龙 | 2009 | 中国循证医学杂志2009，9，7： | 22 |
| 6 | GRADE指南:Ⅸ.证据质量升级显示文摘证据质量升级的最常见原因是效应量大。当方法学严谨的观察性研究表明风险至少降低或增加2倍时,GRADE建议考虑将证据质量升高1级;当风险至少降低或增加5倍时,考虑将证据质量升高2级。当存在剂量-反应关系,或所有合理的混杂、偏倚会降低明显的治疗效应,或混杂、偏倚使得结果无效为假效应时,系统评价作者和指南制定者也可考虑升高证据质量。其他考虑因素包括起效迅速、潜在的疾病(状态)趋势以及间接证据。 | Gordon H.Guyatt Andrew D.Oxman Shahnaz Sultan Paul Glasziou Elie A.Akl Pablo Alonso-Coello David Atkins Regina Kunz Jan Brozek Victor Montori Roman Jaeschke David Rind Philipp Dahm Joerg Meerpohl Gunn Vist Elise Berliner Susan Norris Yngve Falck-Ytter M.Hassan Murad Holger J.Schünemann 代表GRADE工作组 李幼平 杨晓妍 李玲 王应强 | 2011 | 中国循证医学杂志2011，11，12： | 22 |
| 7 | Novel insight into mechanisms of cholestatic liver injury显示文摘Cholestasis results in a buildup of bile acids in serum and in hepatocytes.Early studies into the mechanisms of cholestatic liver injury strongly implicated bile acidinduced apoptosis as the major cause of hepatocellular injury.Recent work has focused both on the role of bile acids in cell signaling as well as the role of sterile inflammation in the pathophysiology.Advances in modern analytical methodology have allowed for more accurate measuring of bile acid concentrations in serum,liver,and bile to very low levels of detection.Interestingly,toxic bile acid levels are seemingly far lower than previously hypothesized.The initial hypothesis has been based largely upon the exposure of μmol/L concentrations of toxic bile acids and bile salts to primary hepatocytes in cell culture,the possibility that in vivo bile acid concentrations may be far lower than the observed in vitro toxicity has far reaching implications in the mechanism of injury.This review will focus on both how different bile acids and different bile acid concentrations can affect hepatocytes during cholestasis,and additionally provide insight into how these data support recent hypotheses that cholestatic liver injury may not occur through direct bile acid-induced apoptosis,but may involve largely inflammatory cell-mediated liver cell necrosis. | Benjamin L Woolbright Hartmut Jaeschke | 2012 | World Journal of Gastroenterology2012，18，36： | 21 |
| 8 | 世界腹腔间隙学会腹内高压和腹腔间隙综合征2013版专家共识与诊疗指南显示文摘随着人们对腹内压(intra-abdominal pressure,IAP)的重视,大量研究开始关注腹内高压(intraabdominal hypertension,IAH)和腹腔间隙综合征(abdominal compartment syndrome,ACS).世界腹腔间隙学会(The abdominal compartment society,WSACS)先后在2006年提出了IAH和ACS的专家共识,2007年发表了诊疗指南,2009年明确了疾病相关研究的推荐方向.2013年WSACS发布了新的IAH和ACS专家共识与诊疗指南.该指南由多学科专家共同参与制定,大部分是外科专家和重症监护专家.专家们首先明确24个临床医师关心的IAH和ACS问题,随后进行了系统有序的文献整理. | Andrew W.Kirkpatrick Derek J.Roberts Jan De Waele Roman Jaeschke Manu L.N.G.Malbrain Bart De Keulenaer Juan Duchesne Martin Bjorc Ari Leppaniemi | 2015 | 中华外科杂志2015，53，3： | 15 |
| 9 | Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012显示文摘 | R. Phillip Dellinger Mitchell M. Levy Andrew Rhodes Djillali Annane Herwig Gerlach Steven M. Opal Jonathan E. Sevransky Charles L. Sprung Ivor S. Douglas Roman Jaeschke Tiffany M. Osborn Mark E. Nunnally Sean R. Townsend Konrad Reinhart Ruth M. Kleinpell | 2013 | Critical Care Medicine2013，，2： | 12 |
| 10 | Mitochondrial dysfunction as a mechanism of drug-induced hepatotoxicity:current understanding and future perspectives显示文摘Mitochondria are critical cellular organelles for energy generation and are now also recognized as playing important roles in cellular signaling.Their central role in energy metabolism,as well as their high abundance in hepatocytes,make them important targets for drug-induced hepatotoxicity.This review summarizes the current mechanistic understanding of the role of mitochondria in drug-induced hepatotoxicity caused by acetaminophen,diclofenac,anti-tuberculosis drugs such as rifampin and isoniazid,anti-epileptic drugs such as valproic acid and constituents of herbal supplements such as pyrrolizidine alkaloids.The utilization of circulating mitochondrialspecific biomarkers in understanding mechanisms of toxicity in humans will also be examined.In summary,it is well-established that mitochondria are central to acetaminophen-induced cell death.However,the most promising areas for clinically useful therapeutic interventions after acetaminophen toxicity may involve the promotion of adaptive responses and repair processes including mitophagy and mitochondrial biogenesis,In contrast,the limited understanding of the role of mitochondria in various aspects of hepatotoxicity by most other drugs and herbs requires more detailed mechanistic investigations in both animals and humans.Development of clinically relevant animal models and more translational studies using mechanistic biomarkers are critical for progress in this area.Relevance for patients:This review focuses on the role of mitochondrial dysfunction in liver injury mechanisms of clinically important drugs like acetaminophen,diclofenac,rifampicin,isoniazid,amiodarone and others.A better understanding of the mechanisms in animal models and their translation to patients will be critical for the identification of new therapeutic targets. | Anup Ramachandran Luqi Duan Jephte Y.Akakpo Hartmut Jaeschke | 2018 | Journal of Clinical & Translational Research2018，4，1： | 8 |
| 11 | Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012显示文摘 | R. P. Dellinger Mitchell M. Levy Andrew Rhodes Djillali Annane Herwig Gerlach Steven M. Opal Jonathan E. Sevransky Charles L. Sprung Ivor S. Douglas Roman Jaeschke Tiffany M. Osborn Mark E. Nunnally Sean R. Townsend Konrad Reinhart Ruth M. Kleinpell Derek | 2013 | Intensive Care Medicine2013，，2： | 7 |
| 12 | 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 |
| 13 | Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008显示文摘 | R. Phillip Dellinger Mitchell M. Levy Jean M. Carlet Julian Bion Margaret M. Parker Roman Jaeschke Konrad Reinhart Derek C. Angus Christian Brun-Buisson Richard Beale Thierry Calandra Jean-Francois Dhainaut Herwig Gerlach Maurene Harvey John J. Marini Joh | 2008 | Intensive Care Medicine2008，，1： | 7 |
| 14 | Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation显示文摘Background and aim:Overdose of acetaminophen(APAP)leads to liver injury,which is one of the most common causes of liver failure in the United States.We previously demonstrated that pharmacological activation of autophagy protects against APAP-induced liver injury in mice via removal of damaged mitochondria and APAP-adducts(APAP-ADs).Using an image-based high-throughput screening for autophagy modulators,we recently identified that chlorpromazine(CPZ),a dopamine inhibitor used for anti-schizophrenia,is a potent autophagy inducer in vitro.Therefore,the aim of the present study is to determine whether CPZ may protect against APAP-induced liver injury via inducing autophagy.Methods:Wild type C57BL/6J mice were injected with APAP to induce liver injury.CPZ was administrated either at the same time with APAP(co-treatment)or 2 h later after APAP administration(post-treat-ment).Hemotoxyline and eosin(H&E)staining of liver histology,terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling(TUNEL)staining of necrotic cell death as well as serum levels of alanine aminotransferase(ALT)were used to monitor liver injury.Results:We found that CPZ markedly protected against APAP-induced liver injury as demonstrated by decreased serum levels of ALT,liver necrotic areas as well as TUNEL-positive cells in mice that were either co-treated or post-treated with CPZ.Mechanistically,we observed that CPZ increased the number of autolysosomes and decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP.Pharmacological inhibition of autophagy by chloroquine partially weak-ened the protective effects of CPZ against APAP-induced liver injury.Conclusions:Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation. | Yuan Li Hong-Min Ni Hartmut Jaeschke Wen-Xing Ding | 2019 | Liver Research2019，3，1： | 7 |
| 15 | Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology显示文摘Acetaminophen(APAP)overdose is the most common cause of acute liver failure in the United States and mechanisms of liver injury induced by APAP overdose have been the focus of extensive investigation.Studies in the mouse model,which closely reproduces the human condition,have shown that hepatotoxicity is initiated by formation of a reactive metabolite N-acetyl-p-benzoquinone imine(NAPQI),which depletes cellular glutathione and forms protein adducts on mitochondrial proteins.This leads to mitochondrial oxidative and nitrosative stress,accompanied by activation of c-jun N-terminal kinase(JNK)and its translocation to the mitochondria.This then amplifies the mitochondrial oxidant stress,resulting in translocation of Bax and dynamin related protein 1(Drp1)to the mitochondria,which induces mitochondrial fission,and ultimately induction of the mitochondrial membrane permeability transition(MPT).The induction of MPT triggers release of intermembrane proteins such as apoptosis inducing factor(AIF)and endonuclease G into the cytosol and their translocation to the nucleus,causing nuclear DNA fragmentation and activation of regulated necrosis.Though these cascades of events were primarily identified in the mouse model,studies on human hepatocytes and analysis of circulating biomarkers from patients after APAP overdose,indicate that a number of mechanistic events are identical in mice and humans.Circulating biomarkers also seem to be useful in predicting the course of liver injury after APAP overdose in humans and hold promise for significant clinical use in the near future.Relevance for patients:This review focuses on the mechanisms behind APAP-induced hepatotoxicity and the relevance of these to the human pathophysiology.Current investigations on various biomarkers which may be useful in clinical management of APAP overdose patients are also discussed. | Anup Ramachandran Hartmut Jaeschke | 2017 | Journal of Clinical & Translational Research2017，3，1： | 6 |
| 16 | Mechanisms of reperfusion injury after warm ischemia of the liver显示文摘 | Hartmut Jaeschke | 1998 | Journal of Hepato - Biliary - Pancreatic Surgery1998，，4： | 4 |
| 17 | Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008显示文摘 | R Phillip Dellinger Mitchell M. Levy Jean M. Carlet Julian Bion Margaret M. Parker Roman Jaeschke Konrad Reinhart Derek C. Angus Christian Brun-Buisson Richard Beale Thierry Calandra Jean-Francois Dhainaut Herwig Gerlach Maurene Harvey John J. Marini John | 2008 | Critical Care Medicine2008，，1： | 4 |
| 18 | Dual roles of p62/SQSTM1 in the injury and recovery phases of acetaminophen-induced liver injury in mice显示文摘Acetaminophen(APAP)overdose can induce liver injury and is the most frequent cause of acute liver failure in the United States.We investigated the role of p62/SQSTM1(referred to as p62)in APAP-induced liver injury(AILI)in mice.We found that the hepatic protein levels of p62 dramatically increased at 24 h after APAP treatment,which was inversely correlated with the hepatic levels of APAPadducts.APAP also activated mTOR at 24 h,which is associated with increased cell proliferation.In contrast,p62 knockout(KO)mice showed increased hepatic levels of APAP-adducts detected by a specific antibody using Western blot analysis but decreased mTOR activation and cell proliferation with aggravated liver injury at 24 h after APAP treatment.Surprisingly,p62 KO mice recovered from AILI whereas the wild-type mice still sustained liver injury at 48 h.We found increased number of infiltrated macrophages in p62 KO mice that were accompanied with decreased hepatic von Willebrand factor(VWF)and platelet aggregation,which are associated with increased cell proliferation and improved liver injury at 48 h after APAP treatment.Our data indicate that p62 inhibits the late injury phase of AILI by increasing autophagic selective removal of APAP-adducts and mitochondria but impairs the recovery phase of AILI likely by enhancing hepatic blood coagulation. | Hui Qian Qingyun Bai Xiao Yang Jephte Y.Akakpo Lili Ji Li Yang Thomas Rulicke Kurt Zatloukal Hartmut Jaeschke Hong-Min Ni Wen-Xing Ding | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 4 |
| 19 | Recommendations for the use of the acetaminophen hepatotoxicity model for mechanistic studies and how to avoid common pitfalls显示文摘Acetaminophen(APAP)is a widely used analgesic and antipyretic drug,which is safe at therapeutic doses but can cause severe liver injury and even liver failure after overdoses.The mouse model of APAP hepatotoxicity recapitulates closely the human pathophysiology.As a result,this clinically relevant model is frequently used to study mechanisms of drug-induced liver injury and even more so to test potential therapeutic interventions.However,the complexity of the model requires a thorough understanding of the pathophysiology to obtain valid results and mechanistic information that is translatable to the clinic.However,many studies using this model are flawed,which jeopardizes the scientific and clinical relevance.The purpose of this review is to provide a framework of the model where mechanistically sound and clinically relevant data can be obtained.The discussion provides insight into the injury mechanisms and how to study it including the critical roles of drug metabolism,mitochondrial dysfunction,necrotic cell death,autophagy and the sterile inflammatory response.In addition,the most frequently made mistakes when using this model are discussed.Thus,considering these recommendations when studying APAP hepatotoxicity will facilitate the discovery of more clinically relevant interventions. | Hartmut Jaeschke Olamide B.Adelusi Jephte Y.Akakpo Nga T.Nguyen Giselle Sanchez-Guerrero David S.Umbaugh Wen-Xing Ding Anup Ramachandran | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 3 |
| 20 | Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: Lessons learned from acetaminophen hepatotoxicity显示文摘 | Hartmut Jaeschke Mitchell R. McGill Anup Ramachandran | 2012 | Drug Metabolism Reviews2012，，1： | 3 |
您所在的机构暂未开通此部分的功能，请联系管理员