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新研究确定了与肝病和脂肪代谢有关的肝细胞突变

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中西医结合肝病杂志 2021年第11期31卷 1011-1011页

作者： Stanley W. K. Ng Foad j. Rouhani Simon F. Brunner Natalia Brzozowska Federico Abascal Luiza Moore Lia Chappell Daniel Leongamornlert Aleksandra Ivovic Philip Robinson timothy Butler Mathij. A. Sanders Nicholas Williams tim H. H. Coorens j.n Teague Keiran Raine Adam P. Butler Yvette Hooks Beverley Wilson Natalie Birtchnell Michael R. Stratton Iñigo Martincorena Raheleh Rahbari Peter j. Campbell Foad j. Rouhani & Huw Naylor Sarah j. Aitken & Matthew Hoare Sarah j. Aitken & Susan E. Davies Sarah j. Aitken Ming Yang Efterpi Nikitopoulou Christian Frezza Matthew Hoare Cancer Genome Proj.ct Wellcome Sanger Institute Hinxton UK Department of Hematology Erasmus University Medical Center Rotterdam The Netherlands Stem Cell Institute University of Cambridge Cambridge UK Department of Surgery Addenbrooke’s Hospital Cambridge UK CRUK Cambridge Institute Cambridge UK Department of Pathology Addenbrooke’s Hospital Cambridge UK MRC Toxicology Unit University of Cambridge Cambridge UK MRC Cancer Unit University of Cambridge Cambridge UK Department of Medicine University of Cambridge Addenbrooke’s Hospital Cambridge UK

一项来自英国韦尔科姆基金会桑格研究所和剑桥大学等研究机构的研究人员的新研究分析了来自34例患者肝脏样本的1590个基因组,包括健康对照、酒精相关肝病和非酒精性脂肪肝疾病患者的肝脏样本,结果发现ACVR2A、TNRC6B、NEAT1、FOXO1和GP... 详细信息

一项来自英国韦尔科姆基金会桑格研究所和剑桥大学等研究机构的研究人员的新研究分析了来自34例患者肝脏样本的1590个基因组,包括健康对照、酒精相关肝病和非酒精性脂肪肝疾病患者的肝脏样本,结果发现ACVR2A、TNRC6B、NEAT1、FOXO1和GPAM 五个基因在肝病患者的肝细胞中发生了突变,过程如图a所示。而其中的FOXO1、CIDEB、GPAM三个基因是对肝细胞如何代谢脂肪和对胰岛素作出反应有直接影响的基因。

关键词： FOXO1 肝病患者细胞突变肝细胞脂肪代谢胰岛素 GPA 剑桥大学

Nature：大规模研究揭示生命所必需的基因

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现代生物医学进展 2016年第31期16卷 I0002-I0003页

作者： Dickinson, Mary E. Flenniken, Ann M. j., Xiao Teboul, Lydia Wong, Michael D. White, j.cqueline K. Meehan, Terrence F. Weninger, Wolfgang j. Westerberg, Henrik Adissu, Hibret Baker, Candice N. Bower, Lynette Brown, j.mes M. Caddle, L. Brianna Chiani, Francesco Clary, Dave Cleak, j.mes Daly, Mark j. Denegre, j.mes M. Doe, Brendan Dolan, Mary E. Edie, Sarah M. Fuchs, Helmut Gailus-Durner, Valerie Galli, Antonella Gambadoro, Alessia Gallegos, j.an Guo, Shiying Horner, Neil R. Hsu, Chih-Wei j.hnson, Sara j. Kalaga, Sowmya Keith, Lance C. Lanoue, Louise Lawson, Thomas N. Lek, Monkol Mark, Manuel Arschall, Susan M. Mason, j.remy McElwee, Melissa L. Newbigging, Susan Nutter, Lauryl M. j. Peterson, Kevin A. Ramirez-Solis, Ramiro Rowland, Douglas j. Ryder, Edward Samocha, Kaitlin E. Seavitt, j.hn R. Selloum, Mohammed Szoke-Kovacs, Zsombor Tamura, Masaru Trainor, Amanda G. Tudose, Ilinca Wakana, Shigeharu Warren, j.nathan Wendling, Olivia West, David B. Wong, Leeyean Yoshiki, Atsushi MacArthur, Daniel G. Tocchini-Valentini, Glauco P. Gao, Xiang Flicek, Paul Bradley, Allan Skarnes, William C. j.stice, Monica j. Parkinson, Helen E. Moore, Mark Wells, Sara Braun, Robert E. Svenson, Karen L. de Angelis, Martin Hrabe Herault, Yann Mohun, tim Mallon, Ann-Marie Henkelman, R. Mark Brown, Steve D. M. Adams, David j. Lloyd, K. C. Kent McKerlie, Colin Beaudet, Arthur L. Bucan, Maj. Murray, Stephen A. Dept Mol Physiol & Biophys Houston TX 77030 USA Toronto Ctr Phenogen Toronto ON M5T 3H7 Canada Mt Sinai Hosp Toronto ON M5G 1X5 Canada Univ Penn Perelman Sch Med Genom & Computat Biol Program Philadelphia PA 19104 USA Med Res Council Harwell Mammalian Genet Unit Harwell OX11 0RD Oxon England Mary Lyon Ctr Harwell OX11 0RD Oxon England Hosp Sick Children Mouse Imaging Ctr Toronto ON M5T 3H7 Canada Wellcome Trust Sanger Inst Wellcome Trust Genome Campus Cambridge CB10 1SA England European Bioinformat Inst European Mol Biol Lab Wellcome Trust Genome Campus Cambridge CB10 1SD England Med Univ Vienna Ctr Anat & Cell Biol A-1090 Vienna Austria Hosp Sick Children 555 Univ Ave Toronto ON M5G 1X8 Canada j.ckson Lab 600 Main St Bar Harbor ME 04609 USA Univ Calif Davis Mouse Biol Program Davis CA 95618 USA Italian Natl Res Council CNR Inst Cell Biol & Neurobiol Monterotondo Mouse Clin I-00015 Monterotondo Italy Massachusetts Gen Hosp Analyt & Translat Genet Unit Boston MA 02114 USA Broad Inst MIT & Harvard Program Med & Populat Genet Cambridge MA 02142 USA German Res Ctr Environm Hlth Helmholtz Zentrum Munchen Inst Expt Genet D-85764 Neuherberg Germany German Mouse Clin D-85764 Neuherberg Germany Baylor Coll Med Dept Mol & Human Genet Houston TX 77030 USA Nanj.ng Univ Nanjing Biomed Res Inst Collaborat Innovat Ctr Genet & Dev SKL Pharmaceut Biotechnol & Model Anim Res Ctr Nanjing 210061 Jiangsu Peoples R China Univ Strasbourg ICS Infrastruct Natl PHENOMIN F-67404 Illkirch Graffenstaden France Univ Strasbourg INSERM CNRS IGBMC F-67404 Illkirch Graffenstaden France RIKEN BioResource Ctr Tsukuba Ibaraki 3050074 Japan Childrens Hosp Oakland Res Inst Oakland CA 94609 USA IMPC San Anselmo CA 94960 USA Tech Univ Munich Sch Life Sci Weihenstephan Chair Expt Genet D-81675 Freising Weihenstephan Germany German Ctr Diabet Res DZD D-85764 Neuherberg Germany Francis Crick Inst Mill Hill Lab Mill Hill London NW1 1AT England Univ Penn Perlman

在哺乳动物基因组中。大约三分之一的基因是生命所必需的。在一项新的研究中，来自美国贝勒医学院等多个机构的研究人员描述了这些基因的大规模发现。以及它将如何影响对哺乳动物发育和人类疾病的理解。相关研究结果在线发表在Nature期... 详细信息

在哺乳动物基因组中。大约三分之一的基因是生命所必需的。在一项新的研究中，来自美国贝勒医学院等多个机构的研究人员描述了这些基因的大规模发现。以及它将如何影响对哺乳动物发育和人类疾病的理解。相关研究结果在线发表在Nature期刊上，论文标题为“High—throughput discovery of novel developmental phenotypes”。

关键词：动物基因组生命哺乳动物研究人员人类疾病医学院

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隐匿性乙型肝炎病毒感染可通过密切接触传播

应用预防医学 2016年第2期22卷 97-101页

作者：胡莉萍刘德平陈钦艳 tim j.Harrison 何翔王学燕李海谭超杨庆利方钟燎广西医科大学基础医学院广西南宁530021 广西崇左市疾病预防控制中心广西壮族自治区疾病预防控制中心广西病毒性肝炎防治研究重点实验室英国伦敦大学学院广东省疾病预防控制中心

目的探索一名出生时乙肝疫苗免疫成功后仍感染乙肝病毒的小孩的感染来源。方法采集小孩及其父母的血标本进行HBV血清学标志物和病毒载量检测,使用酚氯仿法提取HBV DNA,PCR扩增HBV S基因,将扩增产物进行克隆并测序,利用Mega 5.0和Bioedit... 详细信息

目的探索一名出生时乙肝疫苗免疫成功后仍感染乙肝病毒的小孩的感染来源。方法采集小孩及其父母的血标本进行HBV血清学标志物和病毒载量检测,使用酚氯仿法提取HBV DNA,PCR扩增HBV S基因,将扩增产物进行克隆并测序,利用Mega 5.0和Bioedit 7.0对测序结果进行分析。结果父亲和母亲均为隐匿性乙型肝炎病毒感染,父亲、母亲、儿子的PCR产物分别获得12、11和9个克隆株。父亲克隆株的血清型为adrq+,ayw1,ayw,ayr,基因型为C2、B、B/C;母亲克隆株的血清型为ayw1,adw2,adwq+,基因型为C5、B、B/C、C/G;儿子克隆株的血清型为adrq+,基因型仅为C2。S基因序列进化发生树显示,儿子的所有克隆序列与父亲大多数的克隆序列聚集在一起,而与母亲的克隆序列没有聚集。来自儿子和父亲的S基因克隆序列有相同的氨基酸突变模式(T118K、T123N、G145A)。结论儿子乙型肝炎病毒感染的来源是父亲,提示隐匿性乙型肝炎病毒感染可通过家庭密切接触传播。

关键词：乙型肝炎病毒隐匿性感染传播基因变异

Successful treatment of cervical esophageal leakage by endoscopic-vacuum assisted closure therapy

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World j.urnal of Gastrointestinal Endoscopy 2013年第7期5卷 340-345页

作者： Henrike Lenzen Ahmed A Negm Thomas j.Erichsen Michael P Manns j.chen Wedemeyer tim O Lankisch Department of Gastroenterology Hepatology and Endocrinology Hannover Medical School30625 Hannover Germany Department of Internal Medicine Robert Koch Hospital Gehrden30989 Gehrden Germany

AIM: To evaluate the efficacy and safety of endoscopic-vacuum assisted closure (E-VAC) therapy in the treatment of cervical esophageal leakage. METHODS: Between May and November 2012, three male patients who developed post-operative cervical esophageal leakage were treated with E-VAC therapy. One patient had undergone surgical excision of a pharyngo-cervical liposarcoma with partial esophageal resection, and the other two patients had received surgical treatment for symptomatic Zenker's diverticulum. Following endoscopic verification of the leakage, a trimmed polyurethane sponge was fixed to the distal end of a nasogastric silicone tube and endoscopically positioned into the wound cavity, and with decreasing cavity size the sponge was positioned intraluminally to cover the leak. Continuous suction was applied, and the vacuum drainage system was changed twice a ***: The initial E-VAC placement was technically successful for all three patients, and complete closure of the esophageal leak was achieved without any procedure-related complications. In all three patients, the insufficiencies were located either above or slightly below the upper esophageal sphincter. The median duration of the E-VAC drainage was 29 d (range: 19-49 d), with a median of seven sponge exchanges (range: 5-12 sponge exchanges). In addition, the E-VAC therapy reduced inflammatory markers to within normal range for all three patients. Two of the patients were immediately fitted with a percutaneous enteral gastric feeding tube with j.j.nal extension, and the third patient received parenteral feeding. All three patients showed normal swallow function and no evidence of stricture after completion of the E-VAC therapy. CONCLUSION: E-VAC therapy for cervical esophageal leakage was well tolerated by patients. This safe and effective procedure may significantly reduce morbidity and mortality following cervical esophageal leakage.

关键词： Endoscopic-vacuum assisted closure therapy Vacuum therapy Negative pressure wound therapy Cervical esophageal leakage Anastomotic leakage

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运动猝死研究:基于德国全国数据

体育与科学 2016年第3期37卷 44-49页

作者：菲利普·伯姆于尔根·沙尔哈格蒂姆·梅耶张倩任慧涛萨尔大学运动与预防医学学院泉州师范学院体育学院河南大学第一附属医院

(1)背景:与运动有关的心源性猝死(猝死大致分三类,心源性、脑源性和其它,这里一般指心源性运动猝死。下同),不仅经常发生在高水平运动员身上,还频见于非高水平体育竞赛参与者群体。2012年5月,本研究在德国开展,通过对全国范围内运动猝... 详细信息

(1)背景:与运动有关的心源性猝死(猝死大致分三类,心源性、脑源性和其它,这里一般指心源性运动猝死。下同),不仅经常发生在高水平运动员身上,还频见于非高水平体育竞赛参与者群体。2012年5月,本研究在德国开展,通过对全国范围内运动猝死事件的调查,来分析其主要诱因。(2)方法:采用前瞻性研究,通过网络平台搜集、记录并分析案例,并辅以15家法医机构和媒体监测到的案例作为补充。在本研究中,运动相关心源性猝死被界定为:在参与体育运动期间或停止后1小时内出现的死亡(无论复苏成功与否)。研究对象包括不同级别赛事中不同水平的运动员,以及日常体育锻炼参与者。(3)结果:经过30个月的观察,本研究搜集并分析了144个运动猝死样本(平均年龄46.816.2岁)。研究发现,德国运动猝死的总体发病率为每年每百万人1.2至1.5例,其中97%为男性。大多数猝死出现在非高水平体育比赛赛场。足球和跑步是事故发生最多的体育项目。年龄在三十五岁及以下的所有猝死案例中,心肌炎是最常见诱因。年龄在三十五岁以上的的体育参与者猝死中,冠状动脉疾病是主要诱因,也有少量心肌病导致的运动猝死被发现。(4)结论:在德国,运动猝死最大的比例出现于"参与非高水平体育比赛或进行日常体育锻炼的中年男性"群体。欧洲各国运动猝死的主要诱因有所不同。本研究揭示了对参与者进行心脏筛查的重要性。尤其是在非高水平体育竞赛项目开赛之前,应筛查并确认青少年参与者是否患有心肌炎。

关键词：运动员心脏筛查预防猝死

Characterization of the plasma mirror system at the j.KAREN-P facility

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High Power Laser Science and Engineering 2022年第4期10卷 26-35页

作者： Akira Kon Mamiko Nishiuchi Yuj. Fukuda Kotaro Kondo Koichi Ogura Akito Sagisaka Yasuhiro Miyasaka Nicholas P.Dover Masaki Kando Alexander S.Pirozhkov Izuru Daito Liu Chang Il Woo Choi Chang Hee Nam tim Ziegler Hans-Peter Schlenvoigt Karl Zeil Ulrich Schramm Hiromitsu Kiriyama Kansai Photon Science Institute National Institutes for Quantum Science and TechnologyKyoto 619-0215Japan Center for Relativistic Laser Science Institute for Basic ScienceGwangju 61005Republic of Korea Advanced Photonics Research Institute Gwangju Institute of Science and TechnologyGwangju 61005Republic of Korea Department of Physics and Photon Science Gwangju Institute of Science and TechnologyGwangju 61005Republic of Korea Helmholtz-ZentrumDresden-Rossendorf 01328 DresdenGermany Technische Universitat Dresden 01062 DresdenGermany

We report on the design and characterization of the plasma mirror system installed on the j.KAREN-P laser at the Kansai Photon Science Institute,National Institutes for Quantum Science and *** reflectivity of the single plasma mirror system exceeded 80%.In addition,the temporal contrast was improved by two orders of magnitude at 1 ps before the main ***,the laser near-field spatial distribution after the plasma mirror was kept constant at plasma mirror fluence of less than 100 kj.cm^(2).We also present the results of investigating the difference and the fluctuation in energy,pulse width and pointing stability with and without the plasma mirror system.

关键词： high-powerlasers laser plasma plasma mirror

隆安县乙肝病毒无症状携带者HBV前S基因缺失突变的研究

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广西医学 2010年第2期32卷 129-133页

作者：王学燕李国坚董柏青陈钦艳方孔雄杨进业黄坚韦少超方钟燎 Caroline A Sabin tim j.Harrison 广西壮族自治区疾病预防控制中心南宁市530028 广西壮族自治区卫生厅南宁市530021 广西隆安县疾病预防控制中心隆安县532700 英国伦敦大学学院

目的了解肝癌高发区隆安县乙型肝炎病毒(HBV)前S基因缺失突变株的流行情况。方法HBV表面抗原(HBsAg)无症状携带者从我们隆安县研究队列中选择,用套式聚合酶链反应对研究对象血清HBV前S基因扩增和序列分析。结果在66例标本中9例出现前S... 详细信息

目的了解肝癌高发区隆安县乙型肝炎病毒(HBV)前S基因缺失突变株的流行情况。方法HBV表面抗原(HBsAg)无症状携带者从我们隆安县研究队列中选择,用套式聚合酶链反应对研究对象血清HBV前S基因扩增和序列分析。结果在66例标本中9例出现前S基因缺失突变,占13.6%(9/66)。9例缺失突变均为框内突变,其中7例突变发生在或涉及前S2区的5'末端。男6例、女3例出现前S基因缺失突变,但男女间突变率(12.0%,6/50与18.8%,3/16)差异无统计学意义(χ2=0.709,P>0.10);前S基因缺失突变率在基因型B、基因型C和重组基因型之间差异无统计学意义(χ2=0.002,P>0.95)。结论肝癌高发区隆安县居民HBV无症状携带者前S基因缺失突变率较高,这种突变与肝癌的关系值得进一步探讨。

关键词：乙型肝炎病毒表面抗原无症状携带者前S基因缺失突变隆安县

乙肝病毒A1762、G1764双突变是筛选男性HBsAg携带者肝癌最高危人群的生物学标记

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广西医学 2011年第2期33卷 129-132页

作者：王学燕李国坚董柏青杨进业陈钦艳方孔雄黄坚韦少超方钟燎 Caroline A Sabin tim j.Harrison 广西壮族自治区疾病预防控制中心南宁市530028 广西壮族自治区卫生厅南宁市530021 广西隆安县疾病预防控制中心 532700 英国伦敦大学学院

目的探讨乙肝病毒A1762、G1764双突变是否可作为筛选HBsAg携带者肝癌最高危人群的生物学标记。方法对2 258名乙肝病毒无症状携带者进行前瞻性队列研究,其中HBV A1762、G1764双突变株组1 261人,野毒株组997人,跟踪随访队列,每6个月1次对... 详细信息

目的探讨乙肝病毒A1762、G1764双突变是否可作为筛选HBsAg携带者肝癌最高危人群的生物学标记。方法对2 258名乙肝病毒无症状携带者进行前瞻性队列研究,其中HBV A1762、G1764双突变株组1 261人,野毒株组997人,跟踪随访队列,每6个月1次对观察对象抽血进行甲胎蛋白(AFP)检测及B超体检以检查肝癌发病情况。结果观察48个月,2 258名乙肝病毒无症状携带者中,共发生肝癌72例,突变株组64例,野毒株组8例,发病率分别为932.2/10万人年和203.5/10万人年,两组发病率差异有统计学意义(P<0.001),相对危险度(RR)为4.58。突变株组男性发病率1 827.8/10万人年,明显高于野毒株组的180.5/10万人年,两者比较差异有统计学意义(P<0.001),相对危险度为10.13。92.5%的男性病例有双突变;突变株组女性发病率为686.6/10万人年,高于野毒株组的233.3/10万人年,两组比较差异有统计学意义(P<0.05),但相对危险度仅为2.94。结论双突变是筛选男性HBsAg携带者中肝癌最高危人群的很好生物学标记,但对女性筛选肝癌高危人群的意义不如男性。

关键词：乙型肝炎病毒表面抗原无症状携带者 A1762、G1764双突变生物学标记

The phenotype and activation status of regulatory T cells during Friend retrovirus infection

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Virologica Sinica 2014年第1期29卷 48-60页

作者： j.ra j.j.edicke Kirsten K.Dietze Gennadiy Zelinskyy Ulf Dittmer Institute for Virology University Hospital EssenUniversity of Duisburg-Essen

The suppressive capacity of regulatory T cells （Tregs） has been extensively studied and is well established for many *** expansion,accumulation,and activation of Tregs in viral infections are of maj.r interest in order to find ways to alter Treg functions for therapeutic *** are able to dampen effector T cell responses to viral infections and thereby contribute to the establishment of a chronic *** the Friend retrovirus （FV） mouse model,Tregs are known to expand in all infected *** better understand the characteristics of these Treg populations,their phenotype was analyzed in *** acute FV-infection,Tregs became activated in the spleen and bone marrow,as indicated by various T cell activation markers,such as CD43 and ***,Tregs in the bone marrow,which contains the highest viral loads during acute infection,displayed greater levels of activation than Tregs from the *** expansion was driven by proliferation but no FV-specific Tregs could be *** Tregs in FV-infection did not produce Granzyme B （GzmB） or tumor necrosis factor α （TNFα）,which are thought to be a potential mechanism for their suppressive ***,Tregs expressed inhibitory markers,such as tim3,PD-1 and *** tim3 and PD-L1 with antibodies during chronic FV-infection increased the numbers of activated *** data may have important implications for the understanding of Treg functions during chronic viral infections.

关键词： regulatory T cells Friend retrovirus Vβ5+ Treg activation marker