|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | 急性缺血性卒中静脉阿替普酶溶栓治疗的纳入和排除标准的科学依据美国心脏协会/美国卒中协会对医疗卫生专业人员发布的声明(续前)显示文摘19 颅内出血史
根据最初的 FDA 标签和2013年AHA/ASA指南,颅内出血史是静脉阿替普酶治疗缺血性卒中的一项额外禁忌证或排除标准。最近修订后的标签仅将近期 ICH 列为一项警告,并且在禁忌证中删除了ICH史。与前面讨论的静脉阿替普酶治疗排除标准相似,文献回顾仅在大样本回顾性研究中发现了少量这类病例。缺乏相关数据可能是修订后的FDA 标签不再将 ICH 史作为禁忌证而仅将近期ICH 列为一项警告的原因。在这种情况下,FDA 如何定义“近期”一词尚不清楚。有趣的是,对在静脉阿替普酶治疗前通过 MRI 检测脑微出血( cerebral microbleed, CMBs)存在情况进行的研究可为这个卒中亚组患者提供更多的见解。从病理生理学角度,这种微出血的原因尚不清楚,可能反映再灌注损伤或脑血管自动调节功能破坏。因此,在静脉阿替普酶治疗后出现这些损害可能没有意义或是人为信号。 | Dawn O. Kleindorfer Opeolu M. Adeoye Andrew M. Demchuk Jennifer E. Fugate James C. Grotta Alexander A. Khalessi Elad I. Levy Yuko Y. Palesch Shyam Prabhakaran Gustavo Saposnik Jeffrey L. Saver Eric E. Smith 高圆圆 顾雨铖 徐欣 徐曼曼 张佳慧 李韶雅 冒萧萧 陈歆 徐运 | 2016 | 国际脑血管病杂志2016，24，5： | 98 |
| 2 | 限制热量摄入6个月对超重者寿命指标、代谢调节及氧化应激的影响——随机对照试验AuthorAffiliations:PenningtonBiomedicalResearchCenter.LouisianaStateUniversity.BatonRouge;andGarvan.InstituteforMedicalResearch.Dadinghurst,AustraIia(DrHeilbronn).显示文摘背景:长期限制热量摄入可延长啮齿类动物的寿命。但是,尚未有研究观测长期限制人体热量是否会影响其寿命及氧化应激指标,降低代谢率。
目的:在超重但不肥胖(体重指数为25—30)的人群中研究限制热量6个月伴/不伴运动对其产生的影响。
设计、地点及参试者:于2002年3月至2004年8月在位于路易斯安娜州首府巴顿鲁治的研究中心对48名不好动的健康人进行随机对照研究。
干预:参试者在6个月内随机分为4个组:对照组(饮食可维持体重);限制热量组(限制基线所需能量的25%);限制热量+运动组(限制12.5%的热量+运动增加12.5%的能耗);极低热量饮食组(每日摄入890keal,直至体重减少15%,随后采用维持体重的饮食)。
主要观测指标:机体组成;硫酸脱氢表雄酮(dehydroepiandrostemne sulfate,DHEAS)、葡萄糖及胰岛素水平;蛋白羰基化合物;DNA损伤;24小时能耗;核心体温。
结果:6个月时各组体重变化的均值(标准误)为:对照组-1.0%(1.1%);限制热量组-10.4%(0.9%);限制热量+运动组-10.0%(0.8%);极低热量饮食组-13.9%(0.7%)。6个月时,各干预组空腹血糖水平较基线明显降低(P均〈0.01),而DHEAS和葡萄糖水平没有改变。限制热量组及限制热量+运动组核心体温有所下降(P均〈0.05)。对机体组成进行校正后发现,对照组24小时静息能耗无变化,但限制热量组(-135kcal/d[42kcal/d])、限制热量+运动组(-117kcal/d[52kcal/d])和极低热量饮食组(-125kcal/d[35kcal/d])24小时静息能耗有所下降(P均〈0.008)。上述“代谢调节”(超出预计值的-6%)与对照组相比存在显著差异(P〈0.05)。6个月时,各组蛋白羰基化合物的浓度较基线时无变化,而各干预组DNA损伤有所减少(P〈0.005)。
结论:我们的研究结果显示,长期限制热量可降低人类寿命的2种指标(即空腹胰岛素水平和体温)。此外,我们的研究结果还支持下述理论,即限制热量能降低代谢率,且超过缩小代谢面积产生的相应效应。我们尚需开展远期研究来评价限制热量能否延缓人类衰老过程。 | Leonie K. Heibronn Lilian de Jonge Madlyn I. Frisard James P. DeLany D. Enette Larson-Meyer Jennifer Rood Tuong Nguyen Corby K. Martin Julia Volaufova Marlene M. Most Frank L. Greenway Steven R. Smith Walter A. Deutsch Donald A. Williamson Eric Ravussin 顾佳(译) | 2006 | 美国医学会杂志(中文版)2006，25，5： | 18 |
| 3 | Tumor Antigen Specific Activation of Primary Human T-Cells Expressing a Virally Encoded Chimeric T-Cell Receptor Specific for p185HER2显示文摘We have developed and tested chimeric T-cell receptors (TCR) specific for p185HER2. In these experiments, retroviral vectors expressing the N29γ or N29ζ receptors were constructed in pRET6. Amphotropic viral producer cells were established in the GALV-based PG13 packaging cell line. Ficoll purified human peripheral blood lymphocytes (PBL) were virally transduced using an optimized protocol incorporating activation with immobilized anti-CD3/anti-CD28 monoclonal anti- bodies, followed by viral infection in the presence of fibronectin fragment CH296. Transduced cells were co-cultured with human tumor cell lines that overexpress (SK-OV-3) or underexpress (MCF7) p185HER2 to assay for antigen specific im- mune responses. Both CM+ and CD8+ T-cells transduced with the N29γ or N29ζ chTCR demonstrated HER2-specific anti- gen responses, as determined by release of Th1 like cytokines, and cellular cytotoxicity assays. Our results support the fea- sibility of adoptive immunotherapy with genetically modified T-cells expressing a chTCR specific for p185HER2. | 杨建民 Michael S FRIEDMAN Christopher M REYNOLDS Marianne T HUBEN Lee WILKE Jennifer FULLER 李桥 Zelig ESHHAR James J MULE Kevin T MCDONAGH | 2004 | Journal of Microbiology and Immunology2004，2，4： | 5 |
| 4 | Enhancer variants reveal a conserved transcription factor network governed by PU.1 during osteoclast differentiation显示文摘Genome-wide association studies(GWASs) have been instrumental in understanding complex phenotypic traits. However, they have rarely been used to understand lineage-specific pathways and functions that contribute to the trait. In this study, by integrating lineage-specific enhancers from mesenchymal and myeloid compartments with bone mineral density loci, we were able to segregate osteoblast-and osteoclast(OC)-specific functions. Specifically, in OCs, a PU.1-dependent transcription factor(TF)network was revealed. Deletion of PU.1 in OCs in mice resulted in severe osteopetrosis. Functional genomic analysis indicated PU.1 and MITF orchestrated a TF network essential for OC differentiation. Several of these TFs were regulated by cooperative binding of PU.1 with BRD4 to form superenhancers. Further, PU.1 is essential for conformational changes in the superenhancer region of Nfatc1. In summary, our study demonstrates that combining GWASs with genome-wide binding studies and model organisms could decipher lineage-specific pathways contributing to complex disease states. | Heather A.Carey Blake E.Hildreth III Jennifer A.Geisler Mara C.Nickel Jennifer Cabrera Sankha Ghosh Yue Jiang Jing Yan James Lee Sandeep Makam Nicholas A.Young Giancarlo R.Valiente Wael N.Jarjour Kun Huang Thomas J.Rosol Ramiro E.Toribio Julia F.Charles Michael C.Ostrowski Sudarshana M.Sharma | 2018 | Bone Research2018，6，1： | 4 |
| 5 | In vivo anti-tumor activity of murine hematopoietic stem cells expressing a p185HER2-specific chimeric T-cell receptor gene显示文摘We have confirmed efficient anti-tumor activities of the peripheral lymphocytes transduced with a p185HER2-specific chimeric T-cell receptor gene both in murine and in human in our previous studies. To further test the feasibility of chimeric T-cell receptor in a bone marrow transplantation model, we first, made two murine tumor cell lines: MT901 and MCA-205, to express human p185HER2 by retroviral gene transduction. Murine bone marrow cells were retrovirally transduced to express the chimeric T-cell receptor and gene-modified bone marrow cells were transplanted into lethally irradiated mouse. Six months post transplantation, p185HER2-positive tumor cells:MT-901/HER2 or MCA-205/ HER2 was subcutaneously or intravenously injected to make mouse models simulating primary breast cancer or pulmonary metastasis. The in vivo anti-tumor effects were monitored by the size of the subcutaneous tumor or counting the tumor nodules in the lungs after India ink staining. The size of the subcutaneous tumor was significantly inhibited and the number of pulmonary nodules were significantly decreased in mouse recipients transplanted with chimeric T-cell receptor modified bone marrow cells compared with the control group. Our results suggest the efficient in vivo anti-tumor activities of chimeric T-cell receptor gene modified bone marrow cells. | JIAN MIN YANG MICHAEL S FRIEDMAN MARIANNE T HUBEN JENNIFER FULLER QIAO LI ALFRED E CHANG JAMES J MULE KEVIN T MCDONAGH | 2006 | Journal of Microbiology and Immunology2006，4，2： | 3 |
| 6 | Determination of the cellulase activity distribution in Clostridium thermocellum and Caldicellulosiruptor obsidiansis cultures using a fluorescent substrate显示文摘This study took advantage of resorufin cellobioside as a fluorescent substrate to determine the distribution of cellulase activity in cellulosic biomass fermentation systems. Cellulolytic biofilms were found to express nearly four orders greater cellulase activity compared to planktonic cultures of Clostridium thermocellum and Caldicellulosiruptor obsidiansis, which can be primarily attributed to the high cell concentration and surface attachment. The formation of biofilms results in cellulases being secreted close to their substrates, which appears to be an energetically favorable stategy for insoluble substrate utilization. For the same reason,cellulases should be closely associated with the surfaces of suspended cell in soluble substrate-fed culture, which has been verified with cellobiose-fed cultures of C. thermocellum and C. obsidiansis. This study addressed the importance of cellulase activity distribution in cellulosic biomass fermentation, and provided theoretical foundation for the leading role of biofilm in cellulose degradation. System optimization and reactor designs that promote biofilm formation in cellulosic biomass hydrolysis may promise an improved cellulosic biofuel process. | Jennifer L.Morrell-Falvey James G.Elkins Zhi-Wu Wang | 2015 | Journal of Environmental Sciences2015，27，8： | 3 |
| 7 | Endoscopic ultrasound sedation in the United Kingdom: Is life without propofol tolerable?显示文摘There is compelling evidence to support the quality,cost effectiveness and safety profile of non-anesthesiologist-administered propofol for endoscopic ultrasound (EUS). However in the United Kingdom, it is recommended that the administration and monitoring of propofol sedation for endoscopic procedures should be the responsibility of a dedicated and appropriately trained anaesthetist only. The majority of United Kingdom EUS procedures are performed with opiate and benzodiazepine sedation rather than anaesthetist led propofol lists due to anaesthetist resource availability. We sought to prospectively determine the tolerability and safety of EUS with benzodiazepine and opiate sedation in single United Kingdom centre. Two hundred consecutive patients undergoing either EUS or oesophago-gastroduodenoscopy (OGD) with conscious sedation were prospectively recruited with a 1:1 enrolment ratio. Patients completed questionnaires pre and post procedure detailing anticipated and actual pain experienced on a 1-10 visual analogue scale. Demographics, procedure duration, sedation doses and willingness to repeat the procedure were also recorded. EUS procedures lasted significantly longer than OGDs(15 min vs 6 min, P < 0.0001), however, there was no difference in anticipated pain scores between the groups(EUS 3.37/10 vs OGD 3.47/10, P = 0.46). Pain scores indicated EUS was better tolerated than OGD(1.16/10 vs 1.88/10, P = 0.03) although higher doses of sedation were used for EUS procedures. There were no complications identified in either group. We feel our study demonstrates that the tolerability of EUS with opiate and benzodiazepine sedation is acceptable. | Jennifer Anne Campbell Andrew James Irvine Andrew Derek Hopper | 2017 | World Journal of Gastroenterology2017，23，3： | 2 |
| 8 | Telaprevir- and Boceprevir-based Triple Therapy for Hepatitis C in Liver Transplant Recipients With Advanced Recurrent Disease: A Multicenter Study显示文摘 | Elizabeth C. Verna Varun Saxena James R. Burton Jacqueline G. O’Leary Jennifer L. Dodge Richard T. Stravitz Josh Levitsky James F. Trotter Gregory T. Everson Robert S. Brown Norah A. Terrault | 2015 | Transplantation2015，，8： | 2 |
| 9 | Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy显示文摘 | Francesco S. Loffredo Matthew L. Steinhauser Steven M. Jay Joseph Gannon James R. Pancoast Pratyusha Yalamanchi Manisha Sinha Claudia Dall’Osso Danika Khong Jennifer L. Shadrach Christine M. Miller Britta S. Singer Alex Stewart Nikolaos Psychogios Robert | 2013 | Cell2013，，4： | 2 |
| 10 | Exome sequencing reveals genetic architecture in patients with isolated or syndromic short stature显示文摘Short stature is among the most common endocrinological disease phenotypes of childhood and may occur as an isolated finding or in conjunction with other clinical manifestations.Although the diagnostic utility of clinical genetic testing in short stature has been implicated,the genetic architecture and the utility of genomic studies such as exome sequencing(ES)in a sizable cohort of patients with short stature have not been investigated systematically.In this study,we recruited 561 individuals with short stature from two centers in China during a 4-year period.We performed ES for all patients and available parents.All patients were retrospectively divided into two groups:an isolated short stature group(group I,n=257)and an apparently syndromic short stature group(group II,n=304).Causal variants were identified in 135 of 561(24.1%)patients.In group I,29 of 257(11.3%)of the patients were solved by variants in 24 genes.In group II,106 of 304(34.9%)patients were solved by variants in 57 genes.Genes involved in fundamental cellularprocess played an important role in the genetic architecture of syndromic short stature.Distinct genetic architectures and pathophysiological processes underlie isolated and syndromic short stature. | Xin Fan Sen Zhao Chenxi Yu Di Wu Zihui Yan Lijun Fan Yanning Song Yi Wang Chuan Li Yue Ming Baoheng Gui Yuchen Niu Xiaoxin Li Xinzhuang Yang Shiyu Luo Qiang Zhang Xiuli Zhao Hui Pan Mei Li Weibo Xia Guixing Qiu Pengfei Liu Shuyang Zhang Jianguo Zhang Zhihong Wu James R.Lupski Jennifer E.Posey Shaoke Chen Chunxiu Gong Nan Wu | 2021 | Journal of Genetics and Genomics2021，48，5： | 2 |
| 11 | New agents for bacillus Calmette–Guérin-refractory nonmuscle invasive bladder cancer显示文摘 | Jennifer J. Ahn Rashed A. Ghandour James M. McKiernan | 2014 | Current Opinion in Urology2014，，5： | 2 |
| 12 | Factors Related to Inflammation of the Ovarian Epithelium and Risk of Ovarian Cancer显示文摘 | Roberta B. Ness Jeane Ann Grisso Carrie Cottreau Jennifer Klapper Ron Vergona James E. Wheeler Mark Morgan James J. Schlesselman | 2000 | Epidemiology2000，，2： | 2 |
| 13 | 国际卒中遗传学联盟的推荐意见(第2部分):生物样本的采集和储存显示文摘在2003年人类基因组测序以及全基因组基因分型技术发展的共同促进下,人类遗传学的进步已使我们识别出2000多个与性状相关的基因突变。由于这些突变大多数对疾病风险仅有微小的独立影响,因此成功的遗传学研究需要很大的样本量(包含数以千计、万计或者十万计的病例和对照)才能达到足够的研究效能。如此大的样本量积累需要依赖在人类遗传学研究乃至在临床研究中史无前例的大规模国际协作。现在已有许多常见疾病的专病联盟将大量独立机构和合作者联合起来。每个联盟均面临至少2个基本问题:如何整合具有足够数量、同质性和表型质量高的研究样本以及如何储存和分析来自入组受试者的生物样本,有时可能需要在数年间反复进行。 | Thomas W.K.Battey Valerie Valant Sylvia Baedorf Kassis Christina Kourkoulis Chaeyoung Lee Christopher D. Anderson Guido J. Falcone Jordi Jimenez-Conde Israel Fernandez-Cadenas Guillaume Pare Tatjana Rundek Michael L. James Robin Lemmens Tsong-Hai Lee Turgut Tatlisumak Steven J. Kittner Arne Lindgren Farrah J. Mateen Aaron L. Berkowitz Elizabeth G. Holliday Jennifer Majersik 李海峰 姜平 岳耀先 | 2015 | 国际脑血管病杂志2015，23，9： | 2 |
| 14 | NOTUM inhibition increases endocortical bone formation and bone strength显示文摘The disability,mortality and costs caused by non-vertebral osteoporotic fractures are enormous.Existing osteoporosis therapies are highly effective at reducing vertebral but not non-vertebral fractures.Cortical bone is a major determinant of non-vertebral bone strength.To identify novel osteoporosis drug targets,we phenotyped cortical bone of 3 366 viable mouse strains with global knockouts of druggable genes.Cortical bone thickness was substantially elevated in Notum?/?mice.NOTUM is a secreted WNT lipase and we observed high NOTUM expression in cortical bone and osteoblasts but not osteoclasts.Three orally active small molecules and a neutralizing antibody inhibiting NOTUM lipase activity were developed.They increased cortical bone thickness and strength at multiple skeletal sites in both gonadal intact and ovariectomized rodents by stimulating endocortical bone formation.Thus,inhibition of NOTUM activity is a potential novel anabolic therapy for strengthening cortical bone and preventing non-vertebral fractures. | Robert Brommage Jeff Liu Peter Voge Faika Mseeh Andrea Y.Thompson David G.Potter Melanie K.Shadoan Gwenn M.Hansen Sabrina Jeter-Jones Jie Cui Dawn Bright Jennifer P.Bardenhagen Deon D.Doree Sofia Moverare-Skrtic Karin H.Nilsson Petra Henning Ulf H.Lerner Claes Ohlsson Arthur T.Sands James E.Tarver David R.Powell Brian Zambrowicz Qingyun Liu | 2019 | Bone Research2019，7，1： | 2 |
| 15 | You Are What They Eat: The Influence of Reference Groups on Consumers’ Connections to Brands显示文摘 | Jennifer Edson Escalas James R. Bettman | 2003 | Journal of Consumer Psychology2003，，3： | 2 |
| 16 | Differential effects of donor and recipient IL28B and DDX58 SNPs on severity of HCV after liver transplantation显示文摘 | Scott W. Biggins James Trotter Jane Gralla James R. Burton Kiran M. Bambha Jennifer Dodge Megan Brocato Linling Cheng Matt McQueen Lisa Forman Michael Chang Igal Kam Gregory Everson Richard A. Spritz Goran Klintmalm Hugo R. Rosen | 2013 | Journal of Hepatology2013，，5： | 2 |
| 17 | Amelioration of collagen-induced arthritis by CD95 (Apo-1/Fas)-ligand gene transfer显示文摘Both rheumatoid arthritis and animal models ofautoimmune arthritis are characterized by hyper-activation of synovial cells and hyperplasia of the synovialmembrane. The activated synovial cells produceinflammatory cytokines and degradative enzymes whichlead to destruction of cartilage and bones. Effectivetreatment of arthritis may require elimination of most orall activated synovial cells. The death factor | Jennifer L.Horton Elena B.Samoilova Thomas A.Judge Laurence A.Turka James M.Wilson | 1997 | 中国实验血液学杂志1997，5，3： | 2 |
| 18 | Evaluation of prenatal risk factors for prediction of outcome in right heart lesions: CVP Score in fetal right heart defects显示文摘 | Ana Luisa Neves Leigh Mathias Marilyn Wilhm Jennifer Leshko Kersti K. Linask Tiago Henriques-Coelho José C. Areias James C. Huhta | 2014 | The Journal of Maternal-Fetal & Neonatal Medicine2014，，14： | 2 |
| 19 | A DNA Replication Mechanism for Generating Nonrecurrent Rearrangements Associated with Genomic Disorders显示文摘 | Jennifer A. Lee Claudia M.B. Carvalho James R. Lupski | 2007 | Cell2007，，7： | 2 |
| 20 | Pancreatic Fistula Following Pancreaticoduodenectomy: Clinical Predictors and Patient Outcomes显示文摘 | C. Max Schmidt Jennifer Choi Emilie S. Powell Constantin T. Yiannoutsos Nicholas J. Zyromski Attila Nakeeb Henry A. Pitt Eric A. Wiebke James A. Madura Keith D. Lillemoe William Jarnagin | 2009 | HPB Surgery2009，，： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员