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485篇 您的检索式:作者名="David F J"
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1CONSORT 2010说明与详述:报告平行对照随机临床试验指南的更新显示文摘大量证据显示随机对照临床试验(randomised controlled trial,RCT)的报告质量不理想。报告不透明,则读者既不能评判试验结果是否真实可靠,也不能从中提取可用于系统综述的信息。最近的方法学分析表明,报告不充分和设计不合理与对治疗效果产生评价偏倚有关。这种系统误差对RCT损害严重,而RCT正是以其能减少或避免偏倚而被视为评价干预措施的金标准。为了提高RCT的报告质量,一个由专家和编辑组成的工作组制定了临床试验报告的统一标准(Consolidated Standards of Reporting Trials,CONSORT)声明。CONSORT声明于1996年首次发表,并于2001年更新。声明由对照检查清单和流程图组成,供作者在报告RCT时使用。许多核心医学期刊和主要国际性编辑组织都已认可CONSORT声明。该声明促进了对RCT的严格评价和解释。2001年,在对CONSORT进行修订时,人们就已经清楚地认识到,解释和说明制定CONSORT声明的原理,有助于研究人员等撰写或评价临床试验报告。一篇CONSORT说明与详述文章于2001年同2001版CONSORT声明一起发表。2007年1月的专家会议之后,对CONSORT声明作了进一步修订并已发表,即'CONSORT2010声明'。这次更新对原版对照检查清单作了文字上的修改,使其更为明晰,并收入了与一些新近才认识到的主题相关的建议,如选择性报告结局产生的偏倚。说明与详述文件旨在加强人们对CONSORT声明的理解、应用和传播,这次也作了大量修订,对每一项新增或更新的清单条目的含义和增改理由进行了解释,提供了优秀的报告实例,还尽可能地提供了相关的经验性研究的参考文献。文中收入了若干流程图实例。'CONSORT2010声明'、其说明与详述文件,以及相关网站(www.consort-statement.org),对于改进随机临床试验报告必将有所裨益。David Moher Sally Hopewell Kenneth F Schulz Victor Montori Peter C Gφtzsche P J Devereaux Diana Elbourne Matthias Egger Douglas G Altman 周庆辉 卞兆祥 刘建平 2010中西医结合学报2010,8,8:318
2Relationship between Fusobacterium nucleatum,inflammatory mediators and microRNAs in colorectal carcinogenesis显示文摘AIM To examine the effect of Fusobacterium nucleatum(F. nucleatum) on the microenvironment of colonic neoplasms and the expression of inflammatory mediators and microRNAs(miRNAs).METHODS Levels of F. nucleatum DNA, cytokine gene mRNA(TLR2, TLR4, NFKB1, TNF, IL1 B, IL6 and IL8), and potentially interacting miRNAs(miR-21-3p, miR-22-3p, mi R-28-5p, miR-34a-5p, miR-135b-5p) were measured by quantitative polymerase chain reaction(qPCR) TaqMan? assays in DNA and/or RNA extracted from the disease and adjacent normal fresh tissues of 27 colorectal adenoma(CRA) and 43 colorectal cancer(CRC) patients. KRAS mutations were detected by direct sequencing and microsatellite instability(MSI) status by multiplex PCR. Cytoscape v3.1.1 was used to construct the postulated miRNA:mRNA interaction network.RESULTS Overabundance of F. nucleatum in neoplastic tissue compared to matched normal tissue was detected in CRA(51.8%) and more markedly in CRC(72.1%). We observed significantly greater expression of TLR4, IL1 B, IL8, and miR-135 b in CRA lesions and TLR2, IL1 B, IL6, IL8, mi R-34 a and miR-135 b in CRC tumours compared to their respective normal tissues. Only two transcripts for miR-22 and miR-28 were exclusively downregulated in CRC tumour samples. The mRNA expression of IL1 B, IL6, IL8 and miR-22 was positively correlated with F. nucleatum quantification in CRC tumours. The mRNA expression of miR-135 b and TNF was inversely correlated. The miRNA:mRNA interaction network suggested that the upregulation of miR-34 a in CRC proceeds via a TLR2/TLR4-dependent response to F. nucleatum. Finally, KRAS mutations were more frequently observed in CRC samples infected with F. nucleatum and were associated with greater expression of miR-21 in CRA, while IL8 was upregulated in MSI-high CRC.CONCLUSION Our findings indicate that F. nucleatum is a risk factor for CRC by increasing the expression of inflammatory mediators through a possible mi RNA-mediated activation of TLR2/TLR4.Marcela Alcantara Proenca Joice Matos Biselli Maysa Succi Fábio Eduardo Severino Gustavo Noriz Berardinelli Alaor Caetano Rui Manuel Reis David J Hughes Ana Elizabete Silva 2018World Journal of Gastroenterology2018,24,47:15
3Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury显示文摘AIM To investigate the hypothesis that exposure to guanidinoacetate(GAA, a potent methyl-group consumer) either alone or combined with ethanol intake for a prolonged period of time would cause more advanced liver pathology thus identifying methylation defects as the initiator and stimulator for progressive liver damage.METHODS Adult male Wistar rats were fed the control or ethanolLieber De Carli diet in the absence or presence of GAA supplementation. At the end of 6 wk of the feeding regimen, various biochemical and histological analyses were conducted. RESULTS Contrary to our expectations, we observed that GAA treatment alone resulted in a histologically normal liver without evidence of hepatosteatosis despite persistence of some abnormal biochemical parameters. This protection could result from the generation of creatine from the ingested GAA. Ethanol treatment for 6 wk exhibited changes in liver methionine metabolism and persistence of histological and biochemical defects as reported before. Further, when the rats were fed the GAA-supplemented ethanol diet, similar histological and biochemical changes as observed after 2 wk of combined treatment, including inflammation, macroand micro-vesicular steatosis and a marked decrease in the methylation index were noted. In addition, rats on the combined treatment exhibited increased liver toxicity and even early fibrotic changes in a subset of animals in this group. The worsening liver pathology could be related to the profound reduction in the hepatic methylation index, an increased accumulation of GAA and the inability of creatine generated to exert its hepato-protective effects in the setting of ethanol.CONCLUSION To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage.Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David J Orlicky Samuel W French Dean J Tuma Kusum K Kharbanda 2016World Journal of Gastroenterology2016,22,38:2
4Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study显示文摘Pierre Fenaux Ghulam J Mufti Eva Hellstrom-Lindberg Valeria Santini Carlo Finelli Aristoteles Giagounidis Robert Schoch Norbert Gattermann Guillermo Sanz Alan List Steven D Gore John F Seymour John M Bennett John Byrd Jay Backstrom Linda Zimmerman David M 2009Lancet Oncology2009,,:2
5Diabetic Retinopathy显示文摘Thomas W Gardner David A Antonetti Alistair J Barber Kathryn F LaNoue Steven W Levison 2002Survey of Ophthalmology2002,,:2
6Differential diagnosis in patients with suspected bile acid synthesis defects显示文摘AIM: To investigate the clinical presentations associated with bile acid synthesis defects and to describe identification of individual disorders and diagnostic pitfalls. METHODS: We describe semiquantitative determination of 16 urinary bile acid metabolites by electrospray ionization-tandem mass spectrometry. Sample preparation was performed by solid-phase extraction. The total analysis time was 2 min per sample. We determined bile acid metabolites in 363 patients with suspected defects in bile acid metabolism. RESULTS: Abnormal bile acid metabolites were found in 36 patients. Two patients had bile acid synthesis defects but presented with atypical presentations. In 2 other patients who were later shown to be affected by biliary atresia and cystic fibrosis the profile of bile acid metabolites was initially suggestive of a bile acid synthesis defect. Three adult patients suffered from cerebrotendinous xanthomatosis. Nineteen patients had peroxisomal disorders, and 10 patients had cholestatic hepatopathy of other cause. CONCLUSION: Screening for urinary cholanoids should be done in every infant with cholestatic hepatopathy as well as in children with progressive neurological disease to provide specific therapy.Dorothea Haas Hongying Gan-Schreier Claus-Dieter Langhans Tilman Rohrer Guido Engelmann Maura Heverin David W Russell Peter T Clayton Georg F Hoffmann Jürgen G Okun 2012World Journal of Gastroenterology2012,18,10:2
7Molecular-beacon multiplex real-Time PCR assay for detection of Vibrio cholerae显示文摘ANETA J G DAVID F P 2006Appl Environ Microbiol2006,72,9:1
8Ramsdellite-MnO2 for lithium batteries: The ramsdellite to spinel transformation显示文摘THACKERAY M M ROSSOUW M H GUMMOW R J LILES D C PEARCE K KOCK A D DAVID W I F HULLS S 1993Electrochim Acta1993,38,9:1
9LIGHT, a New Member of the TNF Superfamily, and Lymphotoxin α Are Ligands for Herpesvirus Entry Mediator显示文摘Davide N Mauri Reinhard Ebner Rebecca I Montgomery Kristine D Kochel Timothy C Cheung Guo-Liang Yu Steve Ruben Marianne Murphy Roselyn J Eisenberg Gary H Cohen Patricia G Spear Carl F Ware 1998Immunity1998,,:1
10Gastrointestinal permeability and absorptive capacity in sepsis显示文摘JOHNSTON J D HARVEY C J DAVID F 1996Crit Care Med1996,24,7:1
11High-pressure methane and carbon dioxide adsorption on dry and moisture-equilibrated Pennsylvanian coals显示文摘Krooss B M van Bergen F Gensterblum Y Siemons N Pagnier H J M David P 2002Int J Coal Geol2002,51,2:1
12Development of a core set of SSR markers for the characterization of Gossypium germplasm显示文摘JOHON Z Y David D F Russell J K 2012Euphytica2012,187,2:1
13The skill content of recent technological change: an empirical exploration 显示文摘DAVID H LEVY F MURNANE R J 2003The Quarterly Journal of Economics2003,118,4:1
14Optimizing a priority discipline queueing model using fuzzy set theory 显示文摘MARIA J P DAVID D F 2007Computers and Mathematicals with Applica- tions2007,54,:1
15Scanning probe microscopy显示文摘Colton Richard J Baselt David R Dufrêne Yves F Green John-Bruce D Lee Gil U 1997Chemical Biology1997,1,3:1
16Management of insomnia显示文摘David J Charles F 1997The New England Journal of Medicine1997,336,5:1
17Color and depth-based superpixels for back- ground and object segmentation显示文摘ISLEM J DAVID F 2012Procedia Engineering2012,41,0:1
18Aneurysm packing with hydrocoil embolic system versus platinum coil:initial clinical experience显示文摘 David F Kallmes 2004Am J Neuroradiol2004,25,1:1
19Synthesis and Structural Characterization of the Normal Spinel Li O4显示文摘Thomas M G S R David W I F Goodenough J B 1985Mater Res Bull1985,20,:1
20Functional genomics显示文摘Stanley F Yuji David J L 1999Proc Natl Acad Sci1999,96,:1
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