首页 > 最新文献

Journal of Hepatology最新文献

英文 中文
Reply to correspondence on “Acute kidney Injury in patients with cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) joint multidisciplinary consensus meeting” 对关于 "肝硬化患者急性肾损伤 "的信件的回复:急性病质量倡议(ADQI)和国际腹水俱乐部(ICA)多学科联合共识会议"
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-23 DOI: 10.1016/j.jhep.2024.10.025
Mitra K. Nadim, John A. Kellum, François Durand

Section snippets

Authors’ contribution

MKN, JAK and FD wrote the manuscript and revised it

Financial support

none
章节片段作者贡献MKN、JAK和FD撰写并修改了手稿财务支持无
{"title":"Reply to correspondence on “Acute kidney Injury in patients with cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) joint multidisciplinary consensus meeting”","authors":"Mitra K. Nadim, John A. Kellum, François Durand","doi":"10.1016/j.jhep.2024.10.025","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.025","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors’ contribution</h2>MKN, JAK and FD wrote the manuscript and revised it</section></section><section><section><h2>Financial support</h2>none</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"34 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Stigma Among Chinese Speaking Patients with Non-alcoholic Fatty Liver Disease and Their Providers 华语非酒精性脂肪肝患者及其医护人员的耻辱感
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-23 DOI: 10.1016/j.jhep.2024.10.026
Zobair M. Younossi, Maria Stepanova

Section snippets

Abbreviations

Metabolic dysfunction-associated steatotic liver disease (MASLD), non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), metabolic dysfunction-associated fatty liver disease (MAFLD), non-alcoholic steatohepatitis (NASH), metabolic dysfunction-associated steatohepatitis (MASH)”Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is a very common liver disease in the general population with an especially high

Uncited reference

2.; 3.; 4.; 15..

Funding

No funding was received for this work.

Declaration of Competing Interest

ZMY has received research funding and/or serve as consultant to Intercept, CymaBay, Boehringer Ingelheim, BMS, GSK, NovoNordisk, Ipsen, AstraZeneca, Siemens, Madridgal, Merck and Abbott
章节片段缩写代谢功能障碍相关性脂肪肝(MASLD)、非酒精性脂肪肝(NAFLD)、2 型糖尿病(T2D)、代谢功能障碍相关性脂肪肝(MAFLD)、非酒精性脂肪性肝炎(NASH)、代谢功能障碍相关性脂肪性肝炎(MASH)"代谢功能障碍相关性脂肪性肝病(MASLD),以前称为非酒精性脂肪肝(NAFLD),是普通人群中一种非常常见的肝病,发病率特别高。竞争利益声明ZMY 曾接受 Intercept、CymaBay、勃林格殷格翰、BMS、葛兰素史克、诺和诺德、益普生、阿斯利康、西门子、Madridgal、默克和雅培的研究资助和/或担任其顾问。
{"title":"Stigma Among Chinese Speaking Patients with Non-alcoholic Fatty Liver Disease and Their Providers","authors":"Zobair M. Younossi, Maria Stepanova","doi":"10.1016/j.jhep.2024.10.026","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.026","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Abbreviations</h2>Metabolic dysfunction-associated steatotic liver disease (MASLD), non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), metabolic dysfunction-associated fatty liver disease (MAFLD), non-alcoholic steatohepatitis (NASH), metabolic dysfunction-associated steatohepatitis (MASH)”<u>Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is a very common liver disease in the general population with an especially high</u></section></section><section><section><h2>Uncited reference</h2>2.; 3.; 4.; 15..</section></section><section><section><h2>Funding</h2>No funding was received for this work.</section></section><section><section><h2>Declaration of Competing Interest</h2>ZMY has received research funding and/or serve as consultant to Intercept, CymaBay, Boehringer Ingelheim, BMS, GSK, NovoNordisk, Ipsen, AstraZeneca, Siemens, Madridgal, Merck and Abbott</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"93 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oral-gut microbiome interactions in advanced cirrhosis: characterisation of pathogenic enterotypes and salivatypes, virulence factors and antimicrobial 晚期肝硬化患者口腔-肠道微生物组的相互作用:致病性肠道菌型和唾液菌型、毒力因子和抗菌剂的特征描述
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.jhep.2024.09.046
Sunjae Lee, Bethlehem Arefaine, Neelu Begum, Marilena Stamouli, Elizabeth Witherden, Merianne Mohamad, Azadeh Harzandi, Ane Zamalloa, Haizhuang Cai, Roger Williams, Mike Curtis, Lindsey A. Edwards, Shilpa Chokshi, Adil Mardinoglu, Gordon Proctor, David Moyes, Mark J. McPhail, Debbie L. Shawcross, Mathias Uhlen, Saeed Shoaie, Vishal C. Patel
<h3>Background & Aims</h3>Cirrhosis complications are often triggered by bacterial infections with multidrug-resistant organisms. Alterations in the gut and oral microbiome in decompensated cirrhosis (DC) influence clinical outcomes. We interrogated: (i) gut and oral microbiome community structures, (ii) virulence factors (VFs) and antimicrobial resistance genes (ARGs) and (iii) oral-gut microbial overlap in patients with differing cirrhosis severity.<h3>Methods</h3>15 healthy controls (HC), 26 stable cirrhosis (SC), 46 DC, 14 acute-on-chronic liver failure (ACLF) and 14 with severe infection without cirrhosis (NLS) participated. Metagenomic sequencing was undertaken on paired saliva (S) and faecal (F) samples. ‘Salivatypes’ and ‘enterotypes’ based on genera clustering were assessed against cirrhosis severity and clinical parameters. VFs and ARGs were evaluated in oral and gut niches, and distinct resistotypes identified.<h3>Results</h3>Salivatypes and enterotypes revealed a greater proportion of pathobionts with concomitant reduction in autochthonous genera with increasing cirrhosis severity and hyperammonaemia. Increasing overlap between oral and gut microbiome communities was observed in DC and ACLF vs SC and HCs, independent of antimicrobial, beta-blocker and acid suppressant therapies. Two distinct gut microbiome clusters [ENT2/ENT3] harboured genes encoding for the phosphoenolpyruvate:sugar phosphotransferase system (PTS) system and other VFs in DC and ACLF. Substantial ARGs (oral: 1,218 and gut: 672) were detected [575 common to both sites]. The cirrhosis resistome was distinct, with three oral and four gut resistotypes identified, respectively.<h3>Discussion</h3>The degree of oral-gut microbial community overlap, frequency of VFs and ARGs all increment significantly with cirrhosis severity, with progressive dominance of pathobionts and loss of commensals. Despite similar antimicrobial exposure, patients with DC and ACLF have reduced microbial richness compared to NLS, supporting the additive pathobiological effect of cirrhosis.<h3>Impact and implications</h3>This research underscores the crucial role of microbiome alterations in the progression of cirrhosis in an era of escalating multidrug resistant infections, highlighting the association and potential impact of increased oral-gut microbial overlap, virulence factors, and antimicrobial resistance genes on clinical outcomes. These findings are particularly significant for patients with decompensated cirrhosis and acute-on-chronic liver failure, as they reveal the intricate relationship between microbiome alterations and cirrhosis complications. This is relevant in the context of multidrug-resistant organisms and reduced oral-gut microbial diversity that exacerbate cirrhosis severity, drive hepatic decompensation and complicate treatment. For practical applications, these insights could guide for cirrhosis patients the development of targeted microbiome-based therapeutics and personal
背景& 目的肝硬化并发症往往是由耐多药生物的细菌感染引发的。失代偿期肝硬化(DC)患者肠道和口腔微生物群的变化会影响临床预后。我们研究了:(i) 不同肝硬化严重程度患者的肠道和口腔微生物群落结构;(ii) 毒力因子(VFs)和抗菌药耐药基因(ARGs);(iii) 口腔-肠道微生物重叠。对成对的唾液(S)和粪便(F)样本进行了元基因组测序。根据肝硬化严重程度和临床参数评估了基于菌属聚类的 "唾液型 "和 "肠道型"。结果唾液型和肠道型显示,随着肝硬化严重程度和高氨血症程度的增加,病原菌的比例增加,自生菌属随之减少。在 DC 和 ACLF 与 SC 和 HCs 中观察到口腔和肠道微生物群落之间的重叠越来越多,这与抗菌剂、β-受体阻滞剂和抑酸剂疗法无关。在 DC 和 ACLF 中,两个不同的肠道微生物群[ENT2/ENT3]含有编码磷酸烯醇丙酮酸:糖磷酸转移酶系统(PTS)和其他 VF 的基因。检测到了大量的 ARGs(口腔:1,218 个,肠道:672 个)[575 个基因在两个部位共有]。讨论口腔-肠道微生物群落的重叠程度、VFs 和 ARGs 的频率都随着肝硬化的严重程度而显著增加,病原菌逐渐占据主导地位,共生菌逐渐减少。影响和意义这项研究强调了在多重耐药感染不断升级的时代,微生物组改变在肝硬化进展中的关键作用,突出了口腔-肠道微生物重叠、毒力因子和抗菌药耐药基因增加对临床结果的关联和潜在影响。这些发现对于失代偿期肝硬化和急性-慢性肝衰竭患者尤为重要,因为它们揭示了微生物组改变与肝硬化并发症之间错综复杂的关系。耐多药生物和口腔-肠道微生物多样性减少会加重肝硬化的严重程度,导致肝功能失代偿,并使治疗复杂化,在这种情况下,这些发现具有重要意义。在实际应用中,这些见解可以指导肝硬化患者开发基于微生物组的靶向疗法和个性化抗菌方案,以减轻感染性并发症,从而改善他们的临床疗效。
{"title":"Oral-gut microbiome interactions in advanced cirrhosis: characterisation of pathogenic enterotypes and salivatypes, virulence factors and antimicrobial","authors":"Sunjae Lee, Bethlehem Arefaine, Neelu Begum, Marilena Stamouli, Elizabeth Witherden, Merianne Mohamad, Azadeh Harzandi, Ane Zamalloa, Haizhuang Cai, Roger Williams, Mike Curtis, Lindsey A. Edwards, Shilpa Chokshi, Adil Mardinoglu, Gordon Proctor, David Moyes, Mark J. McPhail, Debbie L. Shawcross, Mathias Uhlen, Saeed Shoaie, Vishal C. Patel","doi":"10.1016/j.jhep.2024.09.046","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.09.046","url":null,"abstract":"&lt;h3&gt;Background &amp; Aims&lt;/h3&gt;Cirrhosis complications are often triggered by bacterial infections with multidrug-resistant organisms. Alterations in the gut and oral microbiome in decompensated cirrhosis (DC) influence clinical outcomes. We interrogated: (i) gut and oral microbiome community structures, (ii) virulence factors (VFs) and antimicrobial resistance genes (ARGs) and (iii) oral-gut microbial overlap in patients with differing cirrhosis severity.&lt;h3&gt;Methods&lt;/h3&gt;15 healthy controls (HC), 26 stable cirrhosis (SC), 46 DC, 14 acute-on-chronic liver failure (ACLF) and 14 with severe infection without cirrhosis (NLS) participated. Metagenomic sequencing was undertaken on paired saliva (S) and faecal (F) samples. ‘Salivatypes’ and ‘enterotypes’ based on genera clustering were assessed against cirrhosis severity and clinical parameters. VFs and ARGs were evaluated in oral and gut niches, and distinct resistotypes identified.&lt;h3&gt;Results&lt;/h3&gt;Salivatypes and enterotypes revealed a greater proportion of pathobionts with concomitant reduction in autochthonous genera with increasing cirrhosis severity and hyperammonaemia. Increasing overlap between oral and gut microbiome communities was observed in DC and ACLF vs SC and HCs, independent of antimicrobial, beta-blocker and acid suppressant therapies. Two distinct gut microbiome clusters [ENT2/ENT3] harboured genes encoding for the phosphoenolpyruvate:sugar phosphotransferase system (PTS) system and other VFs in DC and ACLF. Substantial ARGs (oral: 1,218 and gut: 672) were detected [575 common to both sites]. The cirrhosis resistome was distinct, with three oral and four gut resistotypes identified, respectively.&lt;h3&gt;Discussion&lt;/h3&gt;The degree of oral-gut microbial community overlap, frequency of VFs and ARGs all increment significantly with cirrhosis severity, with progressive dominance of pathobionts and loss of commensals. Despite similar antimicrobial exposure, patients with DC and ACLF have reduced microbial richness compared to NLS, supporting the additive pathobiological effect of cirrhosis.&lt;h3&gt;Impact and implications&lt;/h3&gt;This research underscores the crucial role of microbiome alterations in the progression of cirrhosis in an era of escalating multidrug resistant infections, highlighting the association and potential impact of increased oral-gut microbial overlap, virulence factors, and antimicrobial resistance genes on clinical outcomes. These findings are particularly significant for patients with decompensated cirrhosis and acute-on-chronic liver failure, as they reveal the intricate relationship between microbiome alterations and cirrhosis complications. This is relevant in the context of multidrug-resistant organisms and reduced oral-gut microbial diversity that exacerbate cirrhosis severity, drive hepatic decompensation and complicate treatment. For practical applications, these insights could guide for cirrhosis patients the development of targeted microbiome-based therapeutics and personal","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"23 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Increasing functional cure rates after nucleo(s)tide analogue withdrawal: is peg-IFN the answer? 提高核苷酸类似物停药后的功能性治愈率:peg-IFN 是答案吗?
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.jhep.2024.10.019
Edo J. Dongelmans, Milan J. Sonneveld, Harry L.A. Janssen

Section snippets

Clinical trial number:

not applicable.

Conflict of interest:

Edo Dongelmans has no conflicts of interests; Milan Sonneveld receives speakers’ fees and research support from Roche, Bristol Myers Squibb, Gilead Sciences, and Fujirebio. Harry Janssen received grants from: Gilead Sciences, GlaxoSmithKline, Janssen, Roche, Vir Biotechnology Inc. and is consultant for: Aligos, Gilead Sciences, GlaxoSmithKline, Janssen, Roche, Vir Biotechnology Inc., Precision Biosciences, Griffols.

Financial support:

No funding was received for this article.

Author contributions:

Edo Dongelmans, MD (Conceptualization: Equal; Writing – original draft: Lead). Milan Sonneveld, MD, PhD (Conceptualization: Equal; Writing – review & editing: Equal). Harry L.A. Janssen, MD, PhD (Conceptualization: Equal; Supervision: Lead; Writing – review & editing: Equal).

Data availability statement:

not applicable.Nucleo(s)tide analogues (NA) are well-tolerated and highly effective in suppressing HBV DNA in patients with chronic hepatitis B (CHB). Unfortunately, the risk of HCC may persist, particularly in patients who do not achieve functional cure, defined as loss of HBsAg loss. As functional cure is rarely achieved with NA mono-therapy,1 alternative strategies are explored to increase HBsAg clearance.Recent trials with novel compounds suggest that immune modulatory agents likely play a
章节片段临床试验编号:不适用。利益冲突:Edo Dongelmans 没有利益冲突;Milan Sonneveld 从罗氏、百时美施贵宝、吉利德科学公司和 Fujirebio 获得演讲费和研究支持。Harry Janssen 从以下公司获得资助:吉利德科学公司、葛兰素史克公司、杨森公司、罗氏公司、Vir 生物技术公司,并担任以下公司的顾问:作者贡献:Edo Dongelmans,医学博士(构思:Equal;写作-原稿:Lead)。Milan Sonneveld,医学博士(构思:等同;写作 - 审稿 & 编辑:等同)。Harry L.A. Janssen, MD, PhD(构思:等同;指导:等同):平等;指导:撰写-审核-编辑:相同):核苷酸类似物(NA)在抑制慢性乙型肝炎(CHB)患者的 HBV DNA 方面耐受性好、疗效高。遗憾的是,HCC 的风险可能持续存在,尤其是在未达到功能性治愈(即 HBsAg 消失)的患者中。由于 NA 单一疗法很少能实现功能性治愈1 ,因此人们开始探索其他策略来提高 HBsAg 清除率。
{"title":"Increasing functional cure rates after nucleo(s)tide analogue withdrawal: is peg-IFN the answer?","authors":"Edo J. Dongelmans, Milan J. Sonneveld, Harry L.A. Janssen","doi":"10.1016/j.jhep.2024.10.019","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.019","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Clinical trial number:</h2>not applicable.</section></section><section><section><h2>Conflict of interest:</h2>Edo Dongelmans has no conflicts of interests; Milan Sonneveld receives speakers’ fees and research support from Roche, Bristol Myers Squibb, Gilead Sciences, and Fujirebio. Harry Janssen received grants from: Gilead Sciences, GlaxoSmithKline, Janssen, Roche, Vir Biotechnology Inc. and is consultant for: Aligos, Gilead Sciences, GlaxoSmithKline, Janssen, Roche, Vir Biotechnology Inc., Precision Biosciences, Griffols.</section></section><section><section><h2>Financial support:</h2>No funding was received for this article.</section></section><section><section><h2>Author contributions:</h2>Edo Dongelmans, MD (Conceptualization: Equal; Writing – original draft: Lead). Milan Sonneveld, MD, PhD (Conceptualization: Equal; Writing – review &amp; editing: Equal). Harry L.A. Janssen, MD, PhD (Conceptualization: Equal; Supervision: Lead; Writing – review &amp; editing: Equal).</section></section><section><section><h2>Data availability statement:</h2>not applicable.Nucleo(s)tide analogues (NA) are well-tolerated and highly effective in suppressing HBV DNA in patients with chronic hepatitis B (CHB). Unfortunately, the risk of HCC may persist, particularly in patients who do not achieve functional cure, defined as loss of HBsAg loss. As functional cure is rarely achieved with NA mono-therapy,<sup>1</sup> alternative strategies are explored to increase HBsAg clearance.Recent trials with novel compounds suggest that immune modulatory agents likely play a</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"115 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Corrigendum to: “A gold mine of information from a deep dive into the liver transcriptome” [J Hepatol (2024) 540-542] 更正:"深度挖掘肝脏转录组的信息金矿》[J Hepatol (2024) 540-542] 更正
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.jhep.2024.10.003
Wajahat Zafar Mehal
It has come to our attention that the following text should have been included in the ‘Financial support’ section of this article: “Dr. Mehal has an appointment at the West Haven VA Medical Center and this work was supported by a US Department of Veterans Office of Research & Development with grant BX003259-05A1”. We apologise for any inconvenience caused.
我们注意到,本文的 "财务支持 "部分应包含以下文字:"Mehal 博士在西黑文退伍军人医疗中心(West Haven VA Medical Center)任职,这项工作得到了美国退伍军人部研究与发展办公室(US Department of Veterans Office of Research & Development)BX003259-05A1 号基金的支持。我们对由此造成的不便深表歉意。
{"title":"Corrigendum to: “A gold mine of information from a deep dive into the liver transcriptome” [J Hepatol (2024) 540-542]","authors":"Wajahat Zafar Mehal","doi":"10.1016/j.jhep.2024.10.003","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.003","url":null,"abstract":"It has come to our attention that the following text should have been included in the ‘Financial support’ section of this article: “Dr. Mehal has an appointment at the West Haven VA Medical Center and this work was supported by a US Department of Veterans Office of Research &amp; Development with grant BX003259-05A1”. We apologise for any inconvenience caused.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"124 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Is MetALD an independent risk factor of all-cause mortality? A meta-analysis of 164,694 individuals from the real world MetALD 是全因死亡率的独立风险因素吗?对现实世界中 164,694 人进行的荟萃分析
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-21 DOI: 10.1016/j.jhep.2024.10.022
Zheng Li, Yali Shen, Zhiping Li, Dan Cao, Yue Hu

Section snippets

Authors' contributions

Zheng Li, Yue Hu, and Dan Cao contributed to the study conception and design. Zheng Li, Yali Shen, Zhiping Li, Dan Cao, and Yue Hu performed data acquisition, analysis, and interpretation. Zheng Li, Yali Shen, and Zhiping Li wrote the initial draft, Yue Hu and Dan Cao revised the manuscript. All authors reviewed and approved the final manuscript.

Data availability statement

The data that support the findings of this study are all included in this article and the supplementary material.

Funding

This work was jointly supported by the National Natural Science Foundation of China (Grant No. 82272746), and the Medical Science and Technology Project of Sichuan Provincial Health Commission (Grant No. 21PJ135).

Declaration of Competing Interest

The authors declare no conflicts of interest.

Acknowledgements

The authors would like to thank Yaqin Zhao, Ningjing Lei (Division of Abdominal Tumor Multimodality Treatment, Cancer Center, West China Hospital, Sichuan University, Chengdu, China), Xi Chen, Qing Liu, and Shihong Nie (Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China) for their valuable help in data collection and data analysis.
章节片段作者贡献Zheng Li、Yue Hu和Dan Cao参与了研究的构思和设计。李铮、沈雅丽、李治平、曹丹和胡玥进行了数据采集、分析和解释。李铮、沈雅丽和李志平撰写了初稿,胡玥和曹丹对稿件进行了修改。本研究得到了国家自然科学基金(批准号:82272746)和四川省卫计委医学科技项目(批准号:21PJ135)的共同资助。致谢作者感谢赵雅琴、雷宁静(四川大学华西医院肿瘤中心腹部肿瘤多模式治疗科)、陈曦、刘青和聂世红(四川大学华西医院肿瘤中心放射肿瘤科)在数据收集和数据分析方面提供的宝贵帮助。
{"title":"Is MetALD an independent risk factor of all-cause mortality? A meta-analysis of 164,694 individuals from the real world","authors":"Zheng Li, Yali Shen, Zhiping Li, Dan Cao, Yue Hu","doi":"10.1016/j.jhep.2024.10.022","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.022","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors' contributions</h2>Zheng Li, Yue Hu, and Dan Cao contributed to the study conception and design. Zheng Li, Yali Shen, Zhiping Li, Dan Cao, and Yue Hu performed data acquisition, analysis, and interpretation. Zheng Li, Yali Shen, and Zhiping Li wrote the initial draft, Yue Hu and Dan Cao revised the manuscript. All authors reviewed and approved the final manuscript.</section></section><section><section><h2>Data availability statement</h2>The data that support the findings of this study are all included in this article and the supplementary material.</section></section><section><section><h2>Funding</h2>This work was jointly supported by the National Natural Science Foundation of China (Grant No. 82272746), and the Medical Science and Technology Project of Sichuan Provincial Health Commission (Grant No. 21PJ135).</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors declare no conflicts of interest.</section></section><section><section><h2>Acknowledgements</h2>The authors would like to thank Yaqin Zhao, Ningjing Lei (Division of Abdominal Tumor Multimodality Treatment, Cancer Center, West China Hospital, Sichuan University, Chengdu, China), Xi Chen, Qing Liu, and Shihong Nie (Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China) for their valuable help in data collection and data analysis.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"66 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Concordance of ctDNA and tissue genomic profiling in advanced biliary tract cancer 晚期胆道癌中ctDNA和组织基因组图谱分析的一致性
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-21 DOI: 10.1016/j.jhep.2024.10.020
Sohyun Hwang, Seonjeong Woo, Beodeul Kang, Haeyoun Kang, Jung Sun Kim, Sung Hwan Lee, Chang Il Kwon, Dong Soo Kyung, Hwang-Phill Kim, Gwangil Kim, Chan Kim, Hong Jae Chon

Background & Aims

Recent advances in molecular profiling enable the identification of potential therapeutic targets for biliary tract cancer (BTC). However, in patients with BTC, molecular profiling is hindered by challenges in obtaining adequate tissue samples. Circulating tumor DNA (ctDNA) may offer an alternative to tissue-based analysis. Here we aimed to assess the concordance between ctDNA and tissue genomic profiling in a large cohort of Asian patients with advanced BTC, and to evaluate the feasibility of liquid biopsy in BTC treatment.

Methods

This study included patients with systemic treatment-naive advanced BTC, treated at CHA Bundang Medical Center between January 2019 and December 2022. We enrolled patients with available baseline tissue-based next-generation sequencing (NGS), and sufficient plasma samples for ctDNA analysis (AlphaLiquid®100 from IMBdx).

Results

Among 102 enrolled patients, 49.0% had intrahepatic cholangiocarcinoma, 26.5% extrahepatic cholangiocarcinoma, and 24.5% gallbladder cancer. The concordance between intra-patient ctDNA and tumor tissue mutations revealed a sensitivity of 84.8%, and positive predictive value of 79.4%. ctDNA revealed targetable alterations in 34.3% of patients—including FGFR2 fusion, IDH1 mutation, microsatellite instability (MSI)-high, ERBB2 amplification, PIK3CA mutations, BRCA1/2 mutations, and MET amplification. Notably, a novel FGFR2-TNS1 fusion was identified in ctDNA, which was not targeted in the tissue NGS panel. A high maximum somatic variant allele frequency in ctDNA was associated with poor prognosis after gemcitabine/cisplatin-based chemotherapy, in terms of both overall survival (p = 6.9 × 10−6) and progression-free survival (p = 3.8 × 10−7).

Conclusions

Among patients with advanced BTC, ctDNA-based genotyping showed acceptable concordance with tissue genomic profiling. Liquid biopsy using ctDNA could be a valuable complement to tissue-based genomic analysis in BTC.

Impact and implications

Our study is the first large-scale investigation of the clinical utility of liquid biopsy, focusing on ctDNA, as an alternative to conventional tumor tissue analysis, among Asian patients with advanced BTC. The results demonstrated acceptable concordance between analysis of ctDNA versus tissue for identifying therapeutic targets and potentially actionable genetic alterations. This indicates that ctDNA analysis can provide critical insights regarding advanced BTC treatment, particularly in cases where it is challenging to obtain or analyze tumor tissue.
背景与ampamp; 目的分子图谱分析的最新进展有助于确定胆道癌(BTC)的潜在治疗靶点。然而,由于难以获得足够的组织样本,BTC 患者的分子图谱分析受到了阻碍。循环肿瘤 DNA(ctDNA)可作为组织分析的替代方法。本研究纳入了2019年1月至2022年12月期间在CHA盆唐医疗中心接受治疗的全身治疗无效的晚期BTC患者。结果102名入组患者中,49.0%患有肝内胆管癌,26.5%患有肝外胆管癌,24.5%患有胆囊癌。34.3%的患者的ctDNA发现了靶向性改变,包括FGFR2融合、IDH1突变、微卫星不稳定性(MSI)-高、ERBB2扩增、PIK3CA突变、BRCA1/2突变和MET扩增。值得注意的是,在ctDNA中发现了一种新型的FGFR2-TNS1融合体,而组织NGS面板并未针对该融合体。结论在晚期 BTC 患者中,基于 ctDNA 的基因分型与组织基因组图谱分析显示出可接受的一致性。影响和意义我们的研究是首次在亚洲晚期 BTC 患者中大规模调查以 ctDNA 为重点的液体活检替代传统肿瘤组织分析的临床实用性。研究结果表明,ctDNA 分析与组织分析在确定治疗靶点和潜在可操作基因改变方面具有可接受的一致性。这表明,ctDNA 分析能为晚期 BTC 治疗提供重要见解,尤其是在难以获得或分析肿瘤组织的情况下。
{"title":"Concordance of ctDNA and tissue genomic profiling in advanced biliary tract cancer","authors":"Sohyun Hwang, Seonjeong Woo, Beodeul Kang, Haeyoun Kang, Jung Sun Kim, Sung Hwan Lee, Chang Il Kwon, Dong Soo Kyung, Hwang-Phill Kim, Gwangil Kim, Chan Kim, Hong Jae Chon","doi":"10.1016/j.jhep.2024.10.020","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.020","url":null,"abstract":"<h3>Background &amp; Aims</h3>Recent advances in molecular profiling enable the identification of potential therapeutic targets for biliary tract cancer (BTC). However, in patients with BTC, molecular profiling is hindered by challenges in obtaining adequate tissue samples. Circulating tumor DNA (ctDNA) may offer an alternative to tissue-based analysis. Here we aimed to assess the concordance between ctDNA and tissue genomic profiling in a large cohort of Asian patients with advanced BTC, and to evaluate the feasibility of liquid biopsy in BTC treatment.<h3>Methods</h3>This study included patients with systemic treatment-naive advanced BTC, treated at CHA Bundang Medical Center between January 2019 and December 2022. We enrolled patients with available baseline tissue-based next-generation sequencing (NGS), and sufficient plasma samples for ctDNA analysis (AlphaLiquid®100 from IMBdx).<h3>Results</h3>Among 102 enrolled patients, 49.0% had intrahepatic cholangiocarcinoma, 26.5% extrahepatic cholangiocarcinoma, and 24.5% gallbladder cancer. The concordance between intra-patient ctDNA and tumor tissue mutations revealed a sensitivity of 84.8%, and positive predictive value of 79.4%. ctDNA revealed targetable alterations in 34.3% of patients—including <em>FGFR2</em> fusion, <em>IDH1</em> mutation, microsatellite instability (MSI)-high, <em>ERBB2</em> amplification, <em>PIK3CA</em> mutations, <em>BRCA1/2</em> mutations, and <em>MET</em> amplification. Notably, a novel <em>FGFR2-TNS1</em> fusion was identified in ctDNA, which was not targeted in the tissue NGS panel. A high maximum somatic variant allele frequency in ctDNA was associated with poor prognosis after gemcitabine/cisplatin-based chemotherapy, in terms of both overall survival (<em>p</em> = 6.9 × 10<sup>−6</sup>) and progression-free survival (<em>p</em> = 3.8 × 10<sup>−7</sup>).<h3>Conclusions</h3>Among patients with advanced BTC, ctDNA-based genotyping showed acceptable concordance with tissue genomic profiling. Liquid biopsy using ctDNA could be a valuable complement to tissue-based genomic analysis in BTC.<h3>Impact and implications</h3>Our study is the first large-scale investigation of the clinical utility of liquid biopsy, focusing on ctDNA, as an alternative to conventional tumor tissue analysis, among Asian patients with advanced BTC. The results demonstrated acceptable concordance between analysis of ctDNA versus tissue for identifying therapeutic targets and potentially actionable genetic alterations. This indicates that ctDNA analysis can provide critical insights regarding advanced BTC treatment, particularly in cases where it is challenging to obtain or analyze tumor tissue.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"221 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Author’s Reply: Pyroptosis in Liver Failure: A Twisted Firestarter 作者回复:肝衰竭中的脓毒症:扭曲的引火物
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-21 DOI: 10.1016/j.jhep.2024.10.021
Vlad TARU, Thomas REIBERGER

Section snippets

Author contributions:

VT and TR both drafted and reviewed the reply letter for intellectual content.

Financial support:

none.

Declaration of Competing Interest:

VT is funded by the Christian-Doppler Research Association and Boehringer Ingelheim RCV GmbH & Co KG (CD10271603); Romanian Ministry of Research, Innovation and Digitalization (PNRR/2022/C9/MCID/I8).TR received grant support from Abbvie, Boehringer Ingelheim, Gilead, Intercept/Advanz Pharma, MSD, Myr Pharmaceuticals, Philips Healthcare, Pliant, Siemens and W. L. Gore & Associates; speaking honoraria from Abbvie, Echosens, Gilead, Intercept/Advanz Pharma, Roche, MSD, W. L. Gore & Associates;
部分片段作者贡献:VT 和 TR 均起草并审阅了回信的知识性内容。财务支持:无。竞争利益声明:VT 由 Christian-Doppler 研究协会和 Boehringer Ingelheim RCV GmbH & Co KG(CD10271603)、罗马尼亚研究、创新和数字化部(PNRR/2022/C9/MCID/I8)资助。TR 获得了 Abbvie、Boehringer Ingelheim、Gilead、Intercept/Advanz Pharma、MSD、Myr Pharmaceuticals、Philips Healthcare、Pliant、Siemens 和 W. L. Gore & Associates 的资助;Abbvie、Echosens、Gilead、Intercept/Advanz Pharma、Roche、MSD 和 W. L. Gore & Associates 提供了演讲酬金;
{"title":"Author’s Reply: Pyroptosis in Liver Failure: A Twisted Firestarter","authors":"Vlad TARU, Thomas REIBERGER","doi":"10.1016/j.jhep.2024.10.021","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.021","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Author contributions:</h2>VT and TR both drafted and reviewed the reply letter for intellectual content.</section></section><section><section><h2>Financial support:</h2>none.</section></section><section><section><h2>Declaration of Competing Interest:</h2>VT is funded by the Christian-Doppler Research Association and Boehringer Ingelheim RCV GmbH &amp; Co KG (CD10271603); Romanian Ministry of Research, Innovation and Digitalization (PNRR/2022/C9/MCID/I8).TR received grant support from Abbvie, Boehringer Ingelheim, Gilead, Intercept/Advanz Pharma, MSD, Myr Pharmaceuticals, Philips Healthcare, Pliant, Siemens and W. L. Gore &amp; Associates; speaking honoraria from Abbvie, Echosens, Gilead, Intercept/Advanz Pharma, Roche, MSD, W. L. Gore &amp; Associates;</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"20 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thyroid hormone receptor-β analogs for the treatment of Metabolic Dysfunction-Associated Steatohepatitis (MASH) 治疗代谢功能障碍相关性脂肪性肝炎(MASH)的甲状腺激素受体-β类似物
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-19 DOI: 10.1016/j.jhep.2024.10.018
Vlad Ratziu, Thomas S. Scanlan, Eveline Bruinstroop
The association between suboptimal thyroid function ((sub)clinical hypothyroidism or low normal thyroid function) and the metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD) is clearly established. Furthermore, in MASLD, thyroid hormones have low intracellular concentrations and the activation of the thyroid hormone receptor (THR) is reduced. Administration of thyroid hormone has been shown to reduce liver triglycerides by stimulating fatty acid disposal through lipophagy and beta-oxidation, and to lower LDL-cholesterol. As thyroid hormone exerts it’s effects in many different organs, including heart and bone, several drug candidates have been developed acting as selective thyromimetics for the THR-β nuclear receptor with potent and targeted liver actions. Importantly, these compounds have reduced affinity for the THR-α nuclear receptor and tissue distribution profiles that differ from endogenous thyroid hormones thereby reducing unwanted cardiovascular side effects. The most advanced compound, resmetirom, is an oral drug that demonstrated, in a large phase 3 trial in MASH patients, the ability to remove liver fat, reduce aminotransferase levels and improve atherogenic dyslipidemia with a good tolerability profile. This translated into histological improvement that led to accelerated approval of this drug for active fibrotic steatohepatitis, a milestone achievement as a first MASH drug.
甲状腺功能不达标((亚)临床甲状腺功能减退症或甲状腺功能低正常)与代谢综合征和代谢功能障碍相关性脂肪肝(MASLD)之间的联系已得到明确证实。此外,在代谢性脂肪肝中,甲状腺激素在细胞内的浓度较低,甲状腺激素受体(THR)的活化程度也降低。研究表明,服用甲状腺激素可以通过噬脂作用和β-氧化作用刺激脂肪酸处置,从而降低肝脏甘油三酯,并降低低密度脂蛋白胆固醇。由于甲状腺激素在包括心脏和骨骼在内的许多不同器官中发挥作用,因此开发出了几种候选药物,它们作为 THR-β 核受体的选择性仿甲状腺药,对肝脏具有强效的靶向作用。重要的是,这些化合物对THR-α核受体的亲和力较低,组织分布特征与内源性甲状腺激素不同,从而减少了不必要的心血管副作用。最先进的化合物resmetirom是一种口服药物,在一项针对MASH患者的大型三期试验中,它被证明能够清除肝脏脂肪,降低转氨酶水平,改善动脉粥样硬化性血脂异常,而且具有良好的耐受性。这转化为组织学上的改善,导致该药加速获批用于治疗活动性纤维化性脂肪性肝炎,作为首个 MASH 药物,这是一项里程碑式的成就。
{"title":"Thyroid hormone receptor-β analogs for the treatment of Metabolic Dysfunction-Associated Steatohepatitis (MASH)","authors":"Vlad Ratziu, Thomas S. Scanlan, Eveline Bruinstroop","doi":"10.1016/j.jhep.2024.10.018","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.018","url":null,"abstract":"The association between suboptimal thyroid function ((sub)clinical hypothyroidism or low normal thyroid function) and the metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD) is clearly established. Furthermore, in MASLD, thyroid hormones have low intracellular concentrations and the activation of the thyroid hormone receptor (THR) is reduced. Administration of thyroid hormone has been shown to reduce liver triglycerides by stimulating fatty acid disposal through lipophagy and beta-oxidation, and to lower LDL-cholesterol. As thyroid hormone exerts it’s effects in many different organs, including heart and bone, several drug candidates have been developed acting as selective thyromimetics for the THR-β nuclear receptor with potent and targeted liver actions. Importantly, these compounds have reduced affinity for the THR-α nuclear receptor and tissue distribution profiles that differ from endogenous thyroid hormones thereby reducing unwanted cardiovascular side effects. The most advanced compound, resmetirom, is an oral drug that demonstrated, in a large phase 3 trial in MASH patients, the ability to remove liver fat, reduce aminotransferase levels and improve atherogenic dyslipidemia with a good tolerability profile. This translated into histological improvement that led to accelerated approval of this drug for active fibrotic steatohepatitis, a milestone achievement as a first MASH drug.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"4 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142450256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The incidence of hepatitis flare and hepatic decompensation after nucleos(t)ide analogue cessation in chronic hepatitis B patients 慢性乙型肝炎患者停用核苷(t)类似物后肝炎复发和肝功能失代偿的发生率
IF 25.7 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2024-10-18 DOI: 10.1016/j.jhep.2024.10.017
Yen-Chun Liu, Yun-Fan Liaw

Section snippets

Authors contribution:

Yen-Chun Liu: manuscript draftingYun-Fan Liaw: Study concept, manuscript revision

Grant support

This study was supported by grants from Chang Gung Medical Research Fund (CMRPG1N0111) and the Prosperous Foundation, Taipei, Taiwan

Conflict of interest

The authors have no financial and personal relationships with other people or organizations that could inappropriately influence (bias) their work.
章节片段作者贡献:Yen-Chun Liu:手稿起草Yun-Fan Liaw:本研究得到了台湾长庚医学研究基金(CMRPG1N0111)和台湾台北繁荣基金会的资助。
{"title":"The incidence of hepatitis flare and hepatic decompensation after nucleos(t)ide analogue cessation in chronic hepatitis B patients","authors":"Yen-Chun Liu, Yun-Fan Liaw","doi":"10.1016/j.jhep.2024.10.017","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.017","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors contribution:</h2>Yen-Chun Liu: manuscript draftingYun-Fan Liaw: Study concept, manuscript revision</section></section><section><section><h2>Grant support</h2>This study was supported by grants from Chang Gung Medical Research Fund (CMRPG1N0111) and the Prosperous Foundation, Taipei, Taiwan</section></section><section><section><h2>Conflict of interest</h2>The authors have no financial and personal relationships with other people or organizations that could inappropriately influence (bias) their work.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"33 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of Hepatology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1