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| 1 | Serial imaging of human embryonic stem-cell engraftment and teratoma formation in live mouse models显示文摘表示为基于 radiopharmaceutical 的成像为生物体之发光成像或 HSV1 thymidine kinase (HSV1-TK ) 编码任何一个萤火虫酶(fLuc ) 的记者 transgene 的 lentiviral 向量的二种新类型被构造监视人的胚胎的干细胞(hESC ) 在在移植以后的活老鼠的嫁接和增长。任何一个 transgene 的组成的表示没在文化改变 hESCs 的性质。我们下次在 SCID 鼠标监视了 teratomas 的形成到测试(1 ) 是否修改基因的 hESCs 维持他们的发展 pluripotency,并且(2 ) 是否支撑了记者基因表示,允许 noninvasive,在一个活鼠标模型的 hESC 衍生物的整个身体的成像。我们在接种以后从修改基因的房间以及野类型的 hESCs 2-4 月的两种类型观察了 teratoma 形成。用一个光成像系统,从 fLuc-transduced hESCs 的生物体之发光容易在在摸得出的肿瘤能被检测以前,长忍受 teratomas 的老鼠被检测。开发一个 noninvasive 成像方法对诊所更容易地可译,我们也利用了 HSV1-TK 和它的特定的底层, 1-(2 鈥 ? deoxy-2 鈥 ?fluoro- 尾 - D-arabinofuranosyl )-5-[125I]iodouracil ([125I ] FIAU ) ,记者 / 探查对。在全身的管理以后,[125I ] FIAU 是仅仅由编码 transgene 的 HSV1-TK 酶的 phosphorylated 并且在 transduced 以内保留(并且移植) 房间,由单个光子的排放允许敏感、量的成像计算了断层摄影术。象这些那样的 Noninvasive 成像方法可以使我们能在实时接受者以内重复地监视移植人的干细胞的存在和分发在上一通过记者基因的表达式长期。 | Martin G Pomper Holly Hammond Xiaobing Yu Zhaohui Ye Catherine A Foss Doris D Lin James J Fox Linzhao Cheng | 2009 | Cell Research2009，19，3： | 9 |
| 2 | Tight junction disruption: Helicobacter pylori and dysregulation of the gastric mucosal barrier显示文摘Long-term chronic infection with Helicobacter pylori(H. pylori) is a risk factor for gastric cancer development. In the multi-step process that leads to gastric cancer,tight junction dysfunction is thought to occur and serve as a risk factor by permitting the permeation of luminal contents across an otherwise tight mucosa. Mechanisms that regulate tight junction function and structure in the normal stomach,or dysfunction in the infected stomach,however,are largely unknown. Although conventional tight junction components are expressed in gastric epithelial cells,claudins regulate paracellular permeability and are likely the target of inflammation or H. pylori itself. There are 27 different claudin molecules,each with unique properties that render the mucosa an intact barrier that is permselective in a way that is consistent with cell physiology. Understanding the architecture of tight junctions in the normal stomach and then changes that occur during infection is important but challenging,because most of the reports that catalog claudin expression in gastric cancer pathogenesis are contradictory. Furthermore,the role of H. pylori virulence factors,such as cytotoxin-associated gene A and vacoulating cytotoxin,in regulating tight junction dysfunction during infection is inconsistent in different gastric cell lines and in vivo,likely because non-gastric epithelial cell cultures were initially used to unravel the details of their effects on the stomach. Hampering further study,as well,is the relative lack of cultured cell models that have tight junction claudins that are consistent with native tissues. This summary will review the current state of knowledge about gastric tight junctions,normally and in H. pylori infection,and make predictions about the consequences of claudin reorganization during H. pylori infection. | Tyler J Caron Kathleen E Scott James G Fox Susan J Hagen | 2015 | World Journal of Gastroenterology2015，21，40： | 7 |
| 3 | Heterogeneity in mouse spasmolytic polypeptide-expressing metaplasia lineages identifies markers of metaplastic progression显示文摘 | Victoria G Weis Josane F Sousa Bonnie J LaFleur Ki Taek Nam Jared A Weis Paul E Finke Nadia A Ameen James G Fox James R Goldenring | 2013 | Gut2013，，9： | 3 |
| 4 | MoS2/metal composite coating deposited by closed-field unbalanced magnetron sputtering: Tribological properties and industrial uses显示文摘 | Fox V Hampshire J Teer D | 1999 | Surf Coat Technol1999，112，13： | 2 |
| 5 | 基于一个大型随机试验预测稳定性心绞痛队列患者死亡、心肌梗死和卒中的危险评分显示文摘目的对需要抗心绞痛治疗并且左心室功能代偿症状稳定的心绞痛患者建立预测全因死亡、心肌梗死和导致致残性卒中的复合危险评分。设计大型多中心临床试验数据的多变量Cox回归分析。背景西欧、以色列、加拿大、澳大利亚和新西兰的心脏专科门诊患者。入选者7311例具有全部需要资料的患者被入选。主要结局的测量指标平均随访4.9年时间内所有原因的死亡、心肌梗死或者致残性卒中。结果1063例患者发生任何原因死亡或者持久性心肌梗死或者致残性卒中。这些复合终点的5年危险性在危险性最低的十分位患者为4%,而在危险性最高的十分位患者为35%。危险评分结合16项临床常规变量的降序排序是:年龄、左心室射血分数、吸烟、白细胞计数、糖尿病、随机血糖浓度、肌酐浓度、既往卒中病史、1周至少1次心绞痛发作、冠状动脉造影发现(如果能够获得)、降脂治疗、QT间期、收缩期血压≥150mmHg、抗心绞痛药物数量、陈旧性心肌梗死以及性别。把这个模型分别应用于任何原因所致的死亡、心肌梗死和卒中进行预测评估,所得的结果相似。危险评分似乎不能预测事件性质(39%的死亡、46%心肌梗死以及15%致残性卒中)或者冠状动脉造影或血管重建率(占29%的患者)。结论该危险评分对客观地决定稳定性心绞痛患者进一步治疗措施以减少重要预后事件发生是有帮助的。该危险评分同样可以用于将来的计划性试验。 | Tim C Clayton Stuart J Pocock Jacobus Lubsen Zoltán Vokó Bridget-Anne Kirwan Keith A A Fox Philip A Poole-Wilson | 2006 | 英国医学杂志中文版2006，9，1： | 2 |
| 6 | 弓形虫感染引起小胶质细胞与神经元的接触以及细胞体周边抑制性突触丧失显示文摘大脑内的感染和炎症会引起神经元连通性和功能的改变。细胞内的原生动物寄生虫,弓形虫,是一种感染脑部的病原体,可引起脑炎和癫痫发作。这种寄生虫的持续感染还与行为改变和发生精神疾病(包括精神分裂症)的风险增加有关。目前来自人类和小鼠模型的研究证据表明,癫痫发作和精神分裂症均由抑制性突触的丧失或功能障碍引起。与此相符,我们最近报道了持续性弓形虫感染改变谷氨酸脱羧酶67(GAD67)的分布,该酶在抑制性突触中催化GABA的合成。这些变化可能反映突触前装置在抑制性神经元中的重新分布或抑制性神经末梢的丧失。为了直接评估后者的可能性,我们采用序列块面扫描电子显微镜(SBFSEM)并量化寄生虫感染后新皮质和海马中的细胞体周边抑制性突触。持续感染不仅导致明显的细胞体周边突触丧失,而且还诱导髓样来源的细胞对神经元细胞体的包封。免疫组织化学、遗传和超微结构分析显示,这些髓样来源的细胞包括活化的小胶质细胞。最后,超微结构分析确定了包膜于细胞体周围神经末梢的髓样来源的细胞,提示它们可能会主动置换或吞噬突触元件。因此,这些结果表明,活化的小胶质细胞有助于寄生虫感染后细胞体周围抑制突触损失,并对于弓形虫的持续感染可能如何导致癫痫发作和精神疾病提供了一种新的机制。 | Carrillo GL Ballard VA Glausen T Boone Z Teamer J Hinkson CL Wohlfert EA Blader IJ Fox MA 杜一星(编译) | 2020 | 神经损伤与功能重建2020，15，3： | 2 |
| 7 | Chronic proliferative hepatitis in A / J Cr mice associated with persistent Helicobacter hepaticus infection: a model of Helicobacter-induced carcinogenesis 显示文摘 | Fox J G Li X Yan L | 1996 | Infect Immun1996，64，5： | 1 |
| 8 | Synthesis,characterization and ctalytic applications of a palladlum-nanoparticle-cored dendrlmer显示文摘 | Gopidas K R Whitesell J K Fox M A | 2003 | Nano Lett2003，3，12： | 1 |
| 9 | Development of a PCR ELISA assay for the identification of Campylobacter jejuni and Campylobacter coli 显示文摘 | SAILS A D FOX A J BOLTON F J | 2001 | Mol Cell Probe2001，15，： | 1 |
| 10 | Normal human tissues,in addition to some tumors, express multiple different CD44 isoforms 显示文摘 | Fox SB Fawcett J Jackson DG | 1994 | Cancer Res1994，54，16： | 1 |
| 11 | Mice lacking inducible nitric oxide synthase develop spontaneous hypercholestemlaemia and aortic atheromas显示文摘 | Ihrig M Dangler C A Fox J G | 2001 | Atherosclerosis2001，156，1： | 1 |
| 12 | Concise review: mesenchymal stem cells: their phenotype, differentiation capacity, immunological features, and potential for homing 显示文摘 | Chamberlain G Fox J Ashton B | 2007 | Stem Cdls2007，25，11： | 1 |
| 13 | Multiple sig- naling pathways promote B lymphocyte stimulator depen- dent B-cell growth and survival显示文摘 | Woodland RT Fox C J Schmidt MR | 2008 | Blood2008，111，2： | 1 |
| 14 | Angiotensin-converting-enzyme inhibitors in stable vascular disease without left ventricular systolic dysfunction or heart failure:a combined analysis of three trials显示文摘 | Dagenais GR Pogue J Fox K | 2006 | Lancet2006，368，9535： | 1 |
| 15 | Fractal feature analysis and classification in medical imaging显示文摘 | CHEN Chi-chang Daponte J S Fox M D | 1989 | IEEE Transactions on Medical Imaging1989，8，2： | 1 |
| 16 | The serine/ threonine kinase Pim-2 is a transcriptionally regulated apopotot-ic inhibitor显示文摘 | FOX C J HAMMERMAN P S CINALLI R M | 2003 | Genes Dev2003，17，15： | 1 |
| 17 | The role of manipulation following total knee replacement显示文摘 | Fox J L Poss R | 1981 | J Bone Joint Surg Am1981，63，3： | 1 |
| 18 | Effect of surface passivation on performance of A1GaN/GaN/Si HEMTs 显示文摘 | BERNAT J JAVORKA P FOX A | 2003 | Solid-State Electronics2003，47，11： | 1 |
| 19 | Detection and quantification of intraperitonealfluid using electrical impedance tomography显示文摘 | Sadleir R J Fox R A | 2001 | IEEE Trans BiomedEng2001，48，4： | 1 |
| 20 | High-salt diet induces Helicobacter pylori colonization in epithelial hyperplasia and parietal cell loss, and enhances helicobacter pylori colonization in C57BL/6 mice显示文摘 | Fox J G Dangler C A Taylor N S | 1999 | Cancer Res1999，59，9： | 1 |
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