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| 1 | 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 |
| 2 | 英国胃肠病学会关于胃癌风险患者的诊断和管理指南显示文摘胃癌预后较差,部分原因在于诊断较晚。胃癌的危险因素包括幽门螺杆菌(H.pylori,HP)感染和胃癌家族史,尤其是遗传性弥漫性胃癌和恶性贫血。胃癌发展的阶段包括慢性胃炎、胃黏膜萎缩(GA)、胃黏膜肠化生(GIM)和异型增生。胃癌早期发现和提高生存率的关键是在内镜检查前以非侵入性方式识别高危人群。然而,尽管生物标志物可能有助于检测慢性萎缩性胃炎,但尚无足够的证据支持其用于人群筛查。高质量内镜检查是胃癌早期发现的重要组成部分,图像增强内镜结合组织病理学活检是GA和GIM最佳的诊断方法,并能准确进行风险分层。按照悉尼标准从胃窦、角切迹、小弯和大弯进行活检,既能明确诊断,也能对胃癌进行风险分层。理想状态应当是在高质量内镜检查中对GA或GIM区域活检。英国属于低危地区,可根据需要接受常规诊断性胃镜检查,但没有足够证据支持筛查,对于广泛GA或GIM的患者,每3年检查内镜。对于胃异型增生和早期癌,只要满足标准,内镜下黏膜切除术或内镜黏膜下剥离术的治疗有效,成功率高,复发率低。 | Matthew Banks David Graham Marnix Jansen TakujiGotoda Sergio Coda Massimiliano di Pietro NoriyaUedo Pradeep Bhandari D Mark Pritchard Ernst J Kuipers Manuel Rodriguez-Justo Marco R Novelli KrishRagunath Neil Shepherd Mario Dinis-Ribeiro 乌雅罕(译) 张冬雪(译) 牛占岳(校) 刘鑫(校) 丁士刚(译/校) | 2020 | 中华胃肠内镜电子杂志2020，7，2： | 10 |
| 3 | Elucidation of the ‘Honeycrisp’ pedigree through haplotype analysis with a multi-family integrated SNP linkage map and a large apple (Malus×domestica) pedigree-connected SNP data set显示文摘The apple(Malus×domestica)cultivar Honeycrisp has become important economically and as a breeding parent.An earlier study with SSR markers indicated the original recorded pedigree of‘Honeycrisp’was incorrect and‘Keepsake’was identified as one putative parent,the other being unknown.The objective of this study was to verify‘Keepsake’as a parent and identify and genetically describe the unknown parent and its grandparents.A multi-family based dense and high-quality integrated SNP map was created using the apple 8 K Illumina Infinium SNP array.This map was used alongside a large pedigree-connected data set from the RosBREED project to build extended SNP haplotypes and to identify pedigree relationships.‘Keepsake’was verified as one parent of‘Honeycrisp’and‘Duchess of Oldenburg’and‘Golden Delicious’were identified as grandparents through the unknown parent.Following this finding,siblings of‘Honeycrisp’were identified using the SNP data.Breeding records from several of these siblings suggested that the previously unreported parent is a University of Minnesota selection,MN1627.This selection is no longer available,but now is genetically described through imputed SNP haplotypes.We also present the mosaic grandparental composition of‘Honeycrisp’for each of its 17 chromosome pairs.This new pedigree and genetic information will be useful in future pedigree-based genetic studies to connect‘Honeycrisp’with other cultivars used widely in apple breeding programs.The created SNP linkage map will benefit future research using the data from the Illumina apple 8 and 20 K and Affymetrix 480 K SNP arrays. | Nicholas P Howard Eric van de Weg David S Bedford Cameron P Peace Stijn Vanderzande Matthew D Clark Soon Li Teh Lichun Cai James J Luby | 2017 | Horticulture Research2017，4，1： | 9 |
| 4 | Nat Genet:单基因突变导致过敏性皮炎的发生显示文摘最近,研究者们鉴定出了一类导致神经性皮炎发生的关键基因突变:CARDll。来自美国NIH过敏与传染病研究所的研究者们通过对四个没有血缘关系的患病家庭进行分析,发现了这一导致疾病产生的基因、 | Chi A Ma, Yuan Zhang, Michael A Weinreich, Jonathan J Lyons, Celeste G Nelson, Thomas DiMaggio, Kelly D Stone, Joshua D Milner Jeffrey R Stinson, Elisa Ruffo, Batsukh Dorjbal, Swadhinya Arjunaraja, Kelsey Voss, Andrew L Snow Jordan K Abbott, Pia J Hauk, Paul R Reynolds, Erwin W Gelfand Elisa Ruffo Salomé Glauzy, Natsuko Yamakawa, Eric Meffre Jennifer Stoddard, Julie Niemela, Sergio D Rosenzweig Yu Zhang, Helen F Matthews Joshua J McElwee Nina Jones Alejandro Palma, Matías Oleastro, Emma Prieto, Andrea R Bernasconi, Geronimo Dubra, Silvia Danielian, Jonathan Zaiat, Marcelo A Marti Brian Kim Megan A Cooper Neil Romberg | 2017 | 现代生物医学进展2017，17，27： | 3 |
| 5 | Macrophage secretory products induce an inflammatory phenotype in hepatocytes显示文摘AIM:To investigate the influence of macrophages on hepatocyte phenotype and function.METHODS:Macrophages were differentiated from THP-1 monocytes via phorbol myristate acetate stimulation and the effects of monocyte or macrophageconditioned medium on HepG2 mRNA and protein expression determined.The in vivo relevance of these findings was confirmed using liver biopsies from 147 patients with hepatitis C virus(HCV)infection.RESULTS:Conditioned media from macrophages,but not monocytes,induced a transient morphological change in hepatocytes associated with upregulation of vimentin(7.8±2.5-fold,P=0.045)and transforming growth factor(TGF)-β1(2.6±0.2-fold,P<0.001)and downregulation of epithelial cadherin(1.7±0.02-fold,P=0.017)mRNA expression.Microarray analysis revealed significant upregulation of lipocalin-2(17-fold,P <0.001)and pathways associated with inflammation,and substantial downregulation of pathways related to hepatocyte function.In patients with chronic HCV,realtime polymerase chain reaction and immunohistochemistry confirmed an increase in lipocalin-2 mRNA(F0 1.0 ±0.3,F1 2.2±0.2,F2 3.0±9.3,F3/4 4.0±0.8,P= 0.003)and protein expression(F1 1.0±0.5,F2 1.3± 0.4,F3/4 3.6±0.4,P=0.014)with increasing liver injury.High performance liquid chromatography-tandem mass spectrometry analysis identified elevated levels of matrix metalloproteinase(MMP)-9 in macrophageconditioned medium,and a chemical inhibitor of MMP-9 attenuated the change in morphology and mRNA expression of TGF-β1(2.9±0.2 vs 1.04±0.1,P<0.001) in macrophage-conditioned media treated HepG2 cells.In patients with chronic HCV infection,hepatic mRNA expression of CD163(F0 1.0±0.2,F1/2 2.8±0.3,F3/4 5.3±1.0,P=0.001)and MMP-9(F0 1.0±0.4,F1/2 2.8±0.3,F3/4 4.1±0.8,P=0.011)was significantly associated with increasing stage of fibrosis.CONCLUSION:Secreted macrophage products alter the phenotype and function of hepatocytes,with increased expression of inflammatory mediators,suggesting that hepatocytes actively participate in liver injury. | Michelle Melino Victoria L Gadd Gene V Walker Richard Skoien Helen D Barrie Dinesh Jothimani Leigh Horsfall Alun Jones Matthew J Sweet Gethin P Thomas Andrew D Clouston Julie R Jonsson Elizabeth E Powell | 2012 | World Journal of Gastroenterology2012，18，15： | 3 |
| 6 | Requirement for cyclin D3 in germinal center formation and function显示文摘第二等的淋巴的纸巾的幼芽的中心(GC ) 对装高亲密关系的体液的有免疫力的回答批评。当多样化他们的抗体基因时,在 GC 以内的 B 房间经历快速的同种细胞的扩大和选择。尽管 GC B 房间采用一个唯一的 proliferative 程序提供这些进程,这通常被相信,很少联系 GC 的房间周期怎么被安排被知道。D 类型 cyclins 组成使房间能对生理的变化作出回应的房间周期引擎的一个重要部件。房间类型 -- 并且 D 类型 cyclins 的发展阶段特定的角色被描述了,但是 cyclin D 要求没在 GC 反应期间被探讨。在这研究,我们报导 cyclin D3 为切换的增长和 Ig 班大部分是非必需的在 vitro 激活的 B 房间。相反,在 Ccnd3 的 GC 开发 ?/ ?老鼠显著地被损害,作为是 T 房间依赖者抗体反应。在 GC 以内,尽管切换, unswitched B 房间被 cyclin D3 inactivation 影响, IgM?水池更严重地被减少。有趣地尽管有 cyclin D2 表示的补偿增加, Ccnd3 的一个重要数字 ?/ ?GC B 房间处于静止 G0 状态积累。最后,尽管 cyclin D3 inactivation 没在 GC B 房间破坏 BCL6 表示,支持 BCL6 overexpression 的效果完全堵住了 GC,建议 cyclin D3 调整 GC 形成的 BCL6 下游地行动。这是 cyclin D3 玩的第一示范在 B 房间开发的 GC 阶段的一个重要、唯一的角色。 | Jonathan U Peled J Jessica Yu Jeganathan Venkatesh Enguang Bi B Belinda Ding Melissa Krupski-Downs Rita Shaknovich Piotr Sicinski Betty Diamond Matthew D Scharff B Hilda Ye | 2010 | Cell Research2010，20，6： | 3 |
| 7 | Senescent human hepatocytes express a unique secretory phenotype and promote macrophage migration显示文摘AIM:To develop a model of stress-induced senescence to study the hepatocyte senescence associated secretory phenotype(SASP).METHODS:Hydrogen peroxide treatment was used to induce senescence in the human Hep G2 hepatocyte cell line.Senescence was confirmed by cytochemical staining for a panel of markers including Ki67,p21,heterochromatin protein 1β,and senescence-associated-β-galactosidase activity.Senescent hepatocytes were characterised by gene expression arrays and quantitative polymerase chain reaction(q PCR),and conditioned media was used in proteomic analyses,a human chemokine protein array,and cell migration assays to characterise the composition and function of the hepatocyte SASP.RESULTS:Senescent hepatocytes induced classical markers of senescence(p21,heterochromatin protein1β,and senescence-associated-β-galactosidase activity);and downregulated the proliferation marker,Ki67.Hepatocyte senescence induced a 4.6-fold increase in total secreted protein(P=0.06)without major alterations in the protein profile.Senescence-induced genes were identified by microarray(Benjamini Hochbergcorrected P<0.05);and,consistent with the increase in secreted protein,gene ontology analysis revealed a significant enrichment of secreted proteins among inducible genes.The hepatocyte SASP included characteristic factors such as interleukin(IL)-8 and IL-6,as well as novel components such as SAA4,IL-32and Fibrinogen,which were validated by q PCR and/or chemokine protein array.Senescent hepatocyteconditioned medium elicited migration of inflammatory(granulocyte-macrophage colony stimulating factor,GM-CSF-derived),but not non-inflammatory(CSF-1-derived)human macrophages(P=0.022),which could contribute to a pro-inflammatory microenvironment in vivo,or facilitate the clearance of senescent cells.CONCLUSION:Our novel model of hepatocyte senescence provides insights into mechanisms by which senescent hepatocytes may promote chronic liver disease pathogenesis. | Katharine M Irvine Richard Skoien Nilesh J Bokil Michelle Melino Gethin P Thomas Dorothy Loo Brian Gabrielli Michelle M Hill Matthew J Sweet Andrew D Clouston Elizabeth E Powell | 2014 | World Journal of Gastroenterology2014，20，47： | 2 |
| 8 | Celiac disease:Management of persistent symptoms in patients on a gluten-free diet显示文摘AIM:To investigate all patients referred to our center with non-responsive celiac disease (NRCD),to establish a cause for their continued symptoms.METHODS:We assessed all patients referred to our center with non-responsive celiac disease over an 18-mo period.These individuals were investigated to establish the eitiology of their continued symptoms.The patients were first seen in clinic where a thorough history and examination were performed with routine blood work including tissue transglutaminase antibody measurement.They were also referred to a specialist gastroenterology dietician to try to identift any lapses in the diet and sources of hidden gluten ingestion.A repeat small intestinal biopsy was also performed and compared to biopsies from the referring hospital where possible.Colonoscopy,lactulose hydrogen breath testing,pancreolauryl testing and computed tomography scan of the abdomen were undertaken if the symptoms persisted.Their clinical progress was followed over a minimum of 2 years.RESULTS:One hundred and twelve consecutive patients were referred with NRCD.Twelve were found not to have celiac disease (CD).Of the remaining 100 patients,45% were not adequately adhering to a strict gluten-free diet,with 24 (53%) found to be inadvertently ingesting gluten,and 21 (47%) admitting noncompliance.Microscopic colitis was diagnosed in 12% and small bowel bacterial overgrowth in 9%.Refractory CD was diagnosed in 9%.Three of these were diagnosed with intestinal lymphoma.After 2 years,78 patients remained well,eight had continuing symptoms,and four had died.CONCLUSION:In individuals with NRCD,a remediable cause can be found in 90%:with continued gluten ingestion as the leading cause.We propose an algorithm for investigation. | David H Dewar Suzanne C Donnelly Simon D McLaughlin Matthew W Johnson H Julia Ellis Paul J Ciclitira | 2012 | World Journal of Gastroenterology2012，18，12： | 2 |
| 9 | Electrospinning of collagen nanofibers 显示文摘 | Matthews J A Wnek G E Simpson D G | 2002 | Biomacromolecules2002，3，2： | 1 |
| 10 | Homeostasis model assessment:insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man显示文摘 | Matthews D R Hosker J P Rudenski A S | 2002 | Diabetes Care2002，25，10： | 1 |
| 11 | Adaptation of HIV-1to human leukocyte antigen class I显示文摘 | Kawashima Y Pfafferott K Frater J Matthews P Payne R Addo M Gatanaga H Fujiwara M Hachiya A Koizumi H Kuse N Oka S Duda A Prendergast A Crawford H Leslie A Brumme Z Brumme C Allen T Brander C Kaslow R Tang J Hunter E Allen S Mulenga J Branch S Roach T John M Mallal S Ogwu A Shapiro R Prado J G Fidler S Weber J Pybus O G Klenerman P Ndung'u T Phillips R Heckerman D Harrigan P R Walker B D Takiguchi M Goulder P | 2009 | Nature2009，458，7238： | 1 |
| 12 | Freeze-thaw-induced changes of the zona pellucida explains decreased rates of fertilization in frozen-thawed mouse oocytes显示文摘 | Carroll J Depypere H Matthews C D | 1990 | Reprod Fertil1990，90，： | 1 |
| 13 | Experimental study of inequality and unpredictability in an artificial cuitural market显示文摘 | MATTHEW J S PETER S D DUNCAN J W | 2006 | Science2006，311，5762： | 1 |
| 14 | Comparison of constructions of irregular Gallager codes 显示文摘 | MacKay D J C Wilson S T Matthew C D | 1999 | IEEE Trans Commun1999，47，10： | 1 |
| 15 | Maximum Cross Correlation Automatic Satellite Image Navigation and Attitude Corrections for Open-Ocean Image Navigation显示文摘 | EMERY W J BALDWIN D MATTHEWS D | 2003 | IEEE Transactions on Geoscience and Remote Sensing2003，41，1： | 1 |
| 16 | Analysis of serial measurements in medical research显示文摘 | Matthews J N S Altman D G CamPell M J | 1990 | BMJ1990，300，6719： | 1 |
| 17 | Digital Models:An Introduction显示文摘 | Matthew J Peluso Stuart D | 2004 | Semin Orthod2004，10，3： | 1 |
| 18 | Microbial community structure and denitrification in a wetland mitigation bank 显示文摘 | electrophoresis analysis of electrophoresis ( TGGE ) in Per'alta A L Matthews J W Kent A D | 2010 | Appl Environ Microbiol2010，76，13： | 1 |
| 19 | Ecological correlates of seed desiccation tolerance in tropical African dryland trees 显示文摘 | Hugh W P Matthew I D Benjamin J F | 2004 | American Journal of Botany2004，91，6： | 1 |
| 20 | Institutional repositories: evaluating the reasons for non-use of Comell University's Installation of DSpaee 显示文摘 | Philip M D Matthew J L | 2007 | D-Lib Magazine2007，13，34： | 1 |
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