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| 1 | 欧洲新生儿呼吸窘迫综合征防治指南-2010版显示文摘呼吸窘迫综合征(RDS)是由于肺表面活性物质(PS)缺乏及肺结构发育不成熟所致,多见于早产儿,自然病程为生后当时或很快发病,并在生后2d内进行性恶化,如不及时治疗,因进行性缺氧和呼吸衰竭而死亡,存活者,在生后2—4d病情开始改善。胎龄越小,RDS发生率越高,2006年EuroNeoStat的数据显示:胎龄23~25周的早产儿RDS发生率为91%, | Sweet DG Carnielli V Greisen G Hallman M Ozek E Plavka R Saugstad OD Simeoni U Speer CP Halliday HL 袁琳(翻译) 陈超(审校) | 2011 | 中华儿科杂志2011，49，1： | 137 |
| 2 | 欧洲早产儿呼吸窘迫综合征防治共识指南(2013版)显示文摘本次指南更新包括了自2010年以来Cochrane系统评价和医学文献中的最新证据,并采纳了一种新的证据评估分级系统(GRADE)。以往关于早期肺表面活性物质和持续气道正压通气治疗的推荐目前拥有了更坚定的循证依据。对产房复苏、稳定生命体征等内容进行了较大扩充。生命体征稳定后的氧疗目前仍存在一定的争议,但是在获得更多的证据之前,血氧饱和度的目标范围不应低于90%,支持治疗对于超早早产儿仍然极为重要。指南对其他注意事项进行了缩减。 | Sweet D Carnielli V Greisen G Hallman M Ozek E Plavka R Saugstad OD Simeoni U Speer CP Halliday HL 王敏婕 袁琳 陈超 | 2014 | 中华儿科杂志2014，52，10： | 34 |
| 3 | 欧洲新生儿呼吸窘迫综合征防治共识显示文摘呼吸窘迫综合征(RDS)是由于肺表面活性物质(PS)缺乏及肺结构发育不成熟所致,多见于早产儿,自然病程为出生当时或生后很快发病,并在生后2d内进行性恶化,如不及时治疗,因进行性缺氧和呼吸衰竭而死亡。存活者出生后2—4d病情开始改善。RDS临床表现早期出现呼吸窘迫如紫绀、呻吟、吸凹和呼吸急促,然后进一步发展为呼吸衰竭,血气分析结果可提示呼吸衰竭的严重性。胸部X线典型的毛玻璃样改变和支气管充气征可以确诊。Vermont Oxford新生儿协作网对RDS的定义为: | Sweet D Bevilacqua G Carnielli V Greisen G Plavka R Didrik Saugstad O Simeoni U Speer CP Valls-I-Soler A Halliday H 袁琳(译) 陈超(译) 杜立中(校) | 2008 | 中华儿科杂志2008，46，1： | 17 |
| 4 | 新教师发展中心筹建的理念、路径与模式——基于对美国东北大学教师发展中心的访谈显示文摘美国的东北大学教师发展中心属于新创立的组织机构,但发展迅速、运行良好、成绩斐然。其核心成果包括三个部分:一是筹建理念。美国不同类型高校的教师发展中心规模差异较大,各中心命名独具匠心,都充分体现出各自的定位、特色与发展诉求。二是结构与功能设置,不同高校的教师发展中心的隶属关系差别很大,但总体上都与专业学院有严格区分。教师发展中心并不一定在二级学院设立分支机构;中心人员具有高度专业化特征,所聘用人员大多受过专业学科训练,学科差异显著,形成互补优势;多数教师发展中心并不从事教学评估工作,突出服务理念;经费来源相对独立,主要从事促进教师教学和职业发展的相关研究,而非专业的学科性研究。三是吸引力和凝聚力提升问题。青年教师培训体系、工作坊、午餐会、研究生培训、在线课程及互助工作坊等具体手段颇具成效。美国很多高校并不强制青年教师入职培训。中国新建立的教师发展中心应注意:如何评价一个中心的好坏;新的教师发展中心成立后可能面临哪些困难及解决路径;建设初期要注意人员聘任的专业化,以及教师发展中心如何在扭转重科研、轻教学状况中发挥作用等。 | 刘进 刘之远 Michael Sweet | 2017 | 高教发展与评估2017，33，2： | 6 |
| 5 | European Consensus Guidelines on the Management of Neonatal Respiratory Distress Syndrome in Preterm Infants - 2013 Update显示文摘 | Sweet David G Carnielli Virgilio Greisen Gorm Hallman Mikko Ozek Eren Plavka Richard Saugstad Ola D Simeoni Umberto Speer Christian P Vento Maximo Halliday Henry L | 2013 | Neonatology2013，，4： | 3 |
| 6 | 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 |
| 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 | 白内障摘除术后的急性眼内炎文献的系统回顾显示文摘目的:确定白内障摘除术后随时间推移报道的急性眼内炎的发生率并探讨可能引起的因素,如白内障手术切口类型。
方法:以白内障摘除术、眼内炎及术后并发症为关键词,对1963—2003年PubMed上的英文文献进行广泛检索。并进行系统性回顾。附加的研究确认为与其相切题的文献和已发表的会议记录。在可能提供的情况下。记录手术方式。对用不同手术切口技术导致眼内炎发展的累计发生率和相关危险度进行评估。用不同切口的技术评估累计眼内炎的发生率与发展眼内炎的相对危险因素。
结果:从4916篇特定且具潜在相关性的引文中对其中215篇涉及眼内炎且符合入选标准的研究进行分析。总共3140650例白内障手术后,累计0.128%发生眼内炎。然而,急性眼内炎的发生率随着时代不同而改变。与过去lO年相比。2000年以来发生率明显升高(相对危险度,2.44;95%可信区间,2.27—2.61)。2000—2003年眼内炎发生率为0.265%。20世纪90年代为0.087%,80年代为0.158%,70年代为0.327%。并且,与1991年及以前相比,1992年以来发生率有上升趋势。手术切口类型似乎是产生显著影响的危险因素,因为1992—2003年中,经透明角膜切口白内障手术后眼内炎发生率为0.189%。与经巩膜切口0.074%(相对危险度,2.55;95%可信区间,1.75—3.71)及经角巩膜缘切口0.062%(相对危险度,3.06;95%可信区间,2.48—3.76)的发生率相比较,手术切口类型似乎是产生显著影响的危险因素。
结论:这一系统回顾显示,与白内障摘除术相关眼内炎的发生率在过去10年中有所上升。其发生频率的上升趋势与当前无缝线透明角膜白内障摘除术的进展相一致。 | Mehran Taban Ashley Behrens Robert L. Newcomb Matthew Y. Nobe Golnaz Saedi Paula M. Sweet Peter J. McDonnell 胡妙妙(译) 蒋幼芹(校) | 2006 | 美国医学会眼科杂志(中文版)2006，18，1： | 2 |
| 9 | 高效液相色谱法测定酶的活性显示文摘3β,20α-羟基甾体脱氢酶(3β,20α-HSD)是和胚胎的发育密切相关的;我们于1987年首次从胎羊血中得到该酶的纯品,并对其有关性质进行了研究。但是繁杂的测酶活方法常常延误研究工作的顺利进行,因此寻求一种简便有效的测定方法是很有意义的。经多次实验,我们成功地将高效液相色谱技术(HPLC)用于3β,20α-HSD的活性测定,大大缩短了测定时间,促进了有关研究工作的顺利进行。本文将介绍这种新的测酶活方法。 | 陈清轩 Leonard O.Rosik Frederick Sweet | 1992 | 色谱1992，10，2： | 2 |
| 10 | Risperidone and 9 -hydroxyrisperidone concentrations are not dependent on age or creatinine clearance among elderly subjects 显示文摘 | Maxwell RA Sweet RA Mulsant BH | 2002 | J Geriatr Psychiatry Neurol2002，15，2： | 1 |
| 11 | Aneurysmal bone cyst:concept,contro-versries,patient presentation ,and imaging显示文摘 | Kransdorf MJ Sweet DE | 1995 | AJR1995，164，： | 1 |
| 12 | BIL- SAT,l: A low-cost, agile, earth observation microsatel- lite for turkey显示文摘 | BRADFORD A GOMES L M SWEETING M | 2003 | Acta astronautica2003，，53： | 1 |
| 13 | Perform-ance Analysis of the Segment npn Anode LIGBT显示文摘 | GREEN D W SWEET M VERSHININ K V | 2005 | ElectronDevices IEEE Transactions on2005，52，11： | 1 |
| 14 | Atmospheric deposition of PAHs,PCBs, and organochlorine pesticides to Corpus Christi Bay, Texas显示文摘 | Park J S Terry L W Sweet S | 2002 | Atmospheric Environment2002，36，： | 1 |
| 15 | Determingtion of Sulfon-amide Residues in the Tissues of Food Animals Using Automated Precolumn Derivatization and Liquid Chromatography with Fluorescence Detection显示文摘 | Salisburk C D C Sweet J C Munro R | 2004 | J AOAC Int2004，87，5： | 1 |
| 16 | Fundamental principles and practices of team based learning 显示文摘 | Michaelsen LK Sweet M | 2008 | Sterling (VA) : Stylus Publishing :2008，931，： | 1 |
| 17 | Managed care per- spective on three new agents for type 2 diabetes显示文摘 | VanDeKoppel S Choe H M Sweet B V | 2008 | J Manag Care Pharm2008，14，4： | 1 |
| 18 | Tributyltin in environmental samples from the Former Derecktor Shipyard, Coddington Cove, Newport RI显示文摘 | Wade T L Sweet S T Quinn J G Cairns R W King J W | 2004 | Environmental Pollution2004，129，2： | 1 |
| 19 | Gastroesophageal Reflux Disease and Obesity. Pathophysiology and Implications for Treatment显示文摘 | Fernando A. M. Herbella Matthew P. Sweet Pietro Tedesco Ian Nipomnick Marco G. Patti | 2007 | Journal of Gastrointestinal Surgery2007，，3： | 1 |
| 20 | Genesis field, gulf of Mexico:recognizing reservoir compartments on geologic and production time scales in deep-water reservoirs显示文摘 | Sweet M L Sumpter L T | 2007 | AAPG Bulletin2007，91，12： | 1 |
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