|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Molecular subtyping and genomic profiling expand precision medicine in refractory metastatic triple-negative breast cancer:the FUTURE trial显示文摘Triple-negative breast cancer(TNBC)is a highly heterogeneous disease,and molecular subtyping may result in improved diagnostic precision and targeted therapies.Our previous study classified TNBCs into four subtypes with putative therapeutic targets.Here,we conducted the FUTURE trial(ClinicalTrials.gov identifer:NCT03805399),a phaseⅠb/Ⅱsubtyping-based and genomic biomarker-guided umbrella trial,to evaluate the efficacy of these targets.Patients with refractory metastatic TNBC were enrolled and stratifed by TNBC subtypes and genomic biomarkers,and assigned to one of these seven arms:(A)pyrotinib with capecitabine,(B)androgen receptor inhibitor with CDK4/6 inhibitor,(C)anti PD-1 with nab-paclitaxel,(D)PARP inhibitor included,(E)and(F)anti-VEGFR included,or(G)mTOR inhibitor with nab paclitaxel.The primary end point was the objective response rate(ORR).We enrolled 69 refractory metastatic TNBC patients with a median of three previous lines of therapy(range,1-8).Objective response was achieved in 20(29.0%,95%confidence interval(CI):18.7%-41.2%)of the 69 intention-to-treat(ITT)patients.Our results showed that immunotherapy(arm C),in particular,achieved the highest ORR(52.6%,95%CI:28.9%-75.6%)in the ITT population.Arm E demonstrated favorable ORR(26.1%,95%C:10.2%-48.4%in the ITT population)but with more high grade(23)adverse events.Somatic mutations of TOP2A and CD8 immunohistochemical score may have the potential to predict immunotherapy response in the immunomodulatory subtype of TNBC.In conclusion,the phaseⅠb/ⅡFUTURE trial suggested a new concept for TNBC treatment,demonstrating the clinical beneft of subtyping-based targeted therapy for refractory metastatic TNBC. | Yi-Zhou Jiang Yin Liu Yi Xiao Xin Hu Lin Jiang Wen-ia Zuo Ding Ma Jiahan Ding Xiaoyu Zhu Jianjun Zou Claire Verschraegen Daniel G.Stover Virginia Kaklamani Zhong-Hua Wang Zhi-Ming Shao | 2021 | Cell Research2021，31，2： | 37 |
| 2 | Efficient Silencing of Endogenous MicroRNAs Using Artificial MicroRNAs in Arabidopsis thaliana显示文摘我们这里报导内长的 microRNAs (miRNAs ) 的表示能是高效地在用人工的 miRNA (amiRNA ) 的 Arabidopsis thaliana (Arabidopsis ) 的 silenced 技术。我们证明设计指向成熟 miRNA 的 amiRNA 对所有 miRNA 家庭成员指导 silencing,而设计指向一个 miRNA 先锋抄本的茎环区域的 amiRNA 对指向的仅仅单个家庭成员指导 silencing。而且,我们的结果显示指向成熟 miRNA 和茎环顺序的 amiRNAs 通过 miRNA 先锋抄本的劈开指导 RNA silencing,它大概在 miRNA 生物的续生说的起始的阶段期间发生在一个植物房间的原子核。这建议小 RNA (sRNA ) 指导了 RNA 在植物的劈开不仅在细胞质,而且在原子核发生。许多植物 miRNA 基因家庭经由定序和生物信息的分析被识别了,,但是,迄今为止,仅仅这些的小 tranche 机能上地由于有效前面或反向的基因工具的缺乏被描绘了。我们的调查结果因此在植物为 miRNA 功能的分析提供一个新、强大的颠倒基因的工具。 | Andrew L. Eamens Claire Agius Nell A. Smith Peter M. Waterhouse Ming-Bo Wang | 2011 | Molecular Plant2011，4，1： | 10 |
| 3 | Resistin mediates the hepatic stellate cell phenotype显示文摘AIM: To describe the role of resistin in liver fibrosis. METHODS: For the in vivo animal study, Sprague Dawley rats were subjected to bile duct ligation (BDL) for 4 wk. Rat liver, adipose tissue (epididymal fat) and serum were analyzed for resistin expression. For the in vitro experiment, rat primary hepatic stellate cells (HSCs) and Kupffer cells (KCs) were used. HSCs were exposed to recombinant resistin, and collagenⅠ, transforming growth factor β1, α smooth muscle actin, tissue inhibitor of metalloproteinase 1 and connective tissue growth factor expression were analyzed. Resistin gene and protein expression was quantified as was the expression of pro-inflammatory cytokines including tumor necrosis factor α (TNFα), interleukin (IL)-1, IL-6, IL-8 and monocyte chemotactic protein-1 (MCP-1). The effects of resistin on HSC proliferation, migration and apoptosis were determined. The effects of resistin on KCs were also investigated. RESULTS: Following BDL, rat epididymal fat and serum rather than liver showed higher resistin expression compared to control rats. In liver, resistin was expressed in quiescent HSCs and KCs. Resistin treatment resulted in enhancement of TNFα , IL-6 , IL-8 and MCP-1 gene expression and increased IL-6 and MCP-1 protein in HSCs. Resistin activated HSC phospho-MAPK/p38, and p38 inhibition diminished IL-6 and MCP-1 expression. Furthermore, resistin facilitated HSC proliferation and migration, but decreased apoptosis which was via an IL-6 and MCP-1 mechanism. Finally, resistin-induced transforming growth factor β1 from KCs enhanced HSC collagenⅠexpression. CONCLUSION: Resistin directly and indirectly modulates HSC behavior towards a more pro-fibrogenic phenotype. | Zhi-Xia Dong Lin Su Joanne Brymora Claire Bird Qing Xie Jacob George Jian-Hua Wang | 2013 | World Journal of Gastroenterology2013，19，28： | 4 |
| 4 | DMP1 prevents osteocyte alterations,FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease显示文摘During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization,but its effects in CKD are unknown.We tested the hypothesis that DMP1 supplementation in CKD would improve bone health,prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes.We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3^-/- mouse model of CKD.Col4a3^-/- mice demonstrated impaired kidney function,reduced bone DMP1 expression,reduced bone mass,altered osteocyte morphology and connectivity,increased osteocyte apoptosis,increased serum FGF23,hyperphosphatemia,left ventricular hypertrophy (LVH),and reduced survival.Genetic or pharmacological supplementation of DMP1 in Col4a3^-/- mice prevented osteocyte apoptosis,preserved osteocyte networks,corrected bone mass,partially lowered FGF23 levels by attenuating NFAT-induced FGF23 transcription,and further increased serum phosphate.Despite impaired kidney function and worsened hyperphosphatemia,DMP1 prevented development of LVH and improved Col4a3^-/- survival.Our data suggest that CKD reduces DMP1 expression,whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD. | Corey Dussold Claire Gerber Samantha White Xueyan Wang Lixin Qi Connor Francis Maralee Capella Guillaume Courbon Jingya Wang Chaoyuan Li Jian Q. Feng Tamara Isakova Myles Wolf Valentin David Aline Martin | 2019 | Bone Research2019，7，2： | 4 |
| 5 | Effects of luteinizing hormone and androgen on the development of rat progenitor Leydig cells in vitro and in vivo显示文摘祖先 Leydig 房间从干细胞被导出。祖先 Leydig 房间的增长和区别显著地在发身期间贡献 Leydig 房间数字。然而,这些过程的规定仍然保持不清楚。现在的学习的目的是决定 luteinizing 荷尔蒙(LH ) 或雄激素是否贡献祖先 Leydig 房间的增长和区别。Fourteen-day-old 男 Sprague-Dawley 老鼠与 NalGlu 被对待 7 天,它是一个释放 gonadotropin 荷尔蒙对手,到在垂体并且这样减少 LH 的分泌物,在睾丸的雄激素。老鼠与 LH 或 7 α 被共同管理; -methyl-nortestosterone (MENT ) 是对由 5 α 的新陈代谢抵抗的雄激素, -reductase 1 在祖先 Leydig 房间,和 LH 或雄激素的随后的效果被测量。3 H-Thymidine 静脉内地也被注入老鼠在祖先 Leydig 房间学习 thymidine 加入。祖先 Leydig 房间被检验。NalGlu 管理由 83 % 减少了祖先 Leydig 房间增长;。另外, LH 或 MENT 处理恢复了 Leydig 房间 proliferative 能力到 73 %或 50 %控制,分别地。增长相关的基因的送信人 RNA 层次用即时 PCR 被测量。Igf1, Lifr, Pdgfra, Bcl2, Ccnd3 和 Pcna 的表示层次是由 MENT 的 upregulated,并且 Pdgfra, Ccnd3 和 Pcna 的那些是由 LH 的 upregulated。LH 和 MENT 在 vitro 刺激了祖先 Leydig 房间的区别。我们断定 LH 和 MENT 涉及调整祖先 Leydig 房间的发展。 | Jing-Jing Guo Xue Ma Claire Q F Wang Yu-Fei Ge Qing-Quan Lian Dianne O Hard Yu-Fei Zhang Qiang Dong Yun-Fei Xu Ren-Shan Ge | 2013 | Asian Journal of Andrology2013，15，5： | 4 |
| 6 | Lipocalin 2 stimulates bone fibroblast growth factor 23 production in chronic kidney disease显示文摘Bone-produced fibroblast growth factor 23(FGF23)increases in response to inflammation and iron deficiency and contributes to cardiovascular mortality in chronic kidney disease(CKD).Neutrophil gelatinase-associated lipocalin(NGAL or lipocalin 2;LCN2 the murine homolog)is a pro-inflammatory and iron-shuttling molecule that is secreted in response to kidney injury and may promote CKD progression.We investigated bone FGF23 regulation by circulating LCN2.At 23 weeks,Col4a3KO mice showed impaired kidney function,increased levels of kidney and serum LCN2,increased bone and serum FGF23,anemia,and left ventricular hypertrophy(LVH).Deletion of Lcn2 in CKD mice did not improve kidney function or anemia but prevented the development of LVH and improved survival in association with marked reductions in serum FGF23.Lcn2 deletion specifically prevented FGF23 elevations in response to inflammation,but not iron deficiency or phosphate,and administration of LCN2 increased serum FGF23 in healthy and CKD mice by stimulating Fgf23 transcription via activation of cAMP-mediated signaling in bone cells.These results show that kidney-produced LCN2 is an important mediator of increased FGF23 production by bone in response to inflammation and in CKD.LCN2 inhibition might represent a potential therapeutic approach to lower FGF23 and improve outcomes in CKD. | Guillaume Courbon Connor Francis Claire Gerber Samantha Neuburg Xueyan Wang Emily Lynch Tamara Isakova Jodie LBabitt Myles Wolf Aline Martin Valentin David | 2021 | Bone Research2021，9，3： | 4 |
| 7 | 胎儿期恰逢1959~1961年饥荒的中国成人精神分裂症的发病率显示文摘背景:精神分裂症是一种常见的中度精神障碍。子宫内营养缺乏可增大患精神分裂症的危险。其主要依据来自1944~1945年荷兰饥饿冬天(Dutch Hunger Winter)研究,当时食品摄入在短期内极剧下降。这项有关饥荒期间受孕人群的大型队列研究显示,发生精神分裂症的危险增大两倍。
目的:确定经受1959~1961年大饥荒的中国人是否有相似的结果。
设计、地点及参试者:发生精神分裂症危险的调查于安徽省芜湖地区进行,这是当初受灾最重的地区之一。对饥荒之前、饥荒期间和饥荒以后出生的人群发病率进行比较。芜湖及其周围6个县是由一所精神病院负责的。对1971~2001年所有的精神病病历记录均进行检查。精神分裂症患者的临床和社会人口学资料由对自然灾害暴露情况不知情的研究者摘录。有关饥荒年出生人数和死亡人数的数据是有效可用的,累积死亡率根据以后的人口学调查进行估计。
主要观测指标:饥荒的证据已经核实,计算未校正的以及对死亡率进行校正后的发生精神分裂症的相对危险度。
结果:安徽省的出生率(每1000人)在饥荒期问降低了约80%,从1958年的28.28降至1959年的20.97、1960年的8.61和1961年的11.06。在饥荒期间出生的人,晚年发生精神分裂症的校正后危险明显增高,从1959年的0.84%增至1960年的2.15%和1961年的1.81%。死亡率校正相对危险在1960年出生者为2.30(95%可信区间,1.99~2.05),1961年出生者为1.93(95%可信区间,1.68~2.23)。
结论:我们的调查重复了荷兰不同种族人群的数据,结果显示,出生前遭受饥荒可增高晚年患精神分裂症的危险。 | David St Clair Mingqing Xu Peng Wang Yaqin Yu Yourong Fang Feng Zhang Xiaoying Zheng Niufan Gu Guoyin Feng Pak Sham Lin He 张继志(译) | 2006 | 美国医学会杂志(中文版)2006，25，4： | 3 |
| 8 | An NgAgo tool for genome editing:did CRISPR/Cas9 just find a competitor?显示文摘While CRISPR/Cas9-mediated genome editing technology has been experiencing a rapid transformation during the past few years,a recent report on NgAgo-mediated singlestranded DNA-guided genome editing may offer an attractive alternative for genome manipulation.While it’s too early to predict whether NgAgo will be able to compete with or be superior to CRISPR/Cas9,the scientific community is anxiously waiting for further optimization and broader applications of the NgAgo genome editing technology. | Qiang Wei Junyi Liao Xinyi Yu Eric J.Wang Claire Wang Hue H.Luu Rex C.Haydon Michael J.Lee Tong-Chuan He | 2016 | Genes & Diseases2016，3，3： | 2 |
| 9 | The Surgical Treatment and Outcome of Nonmetastatic Extremity Osteosarcoma with Pathological Fractures显示文摘 | Zhi-Ping Deng Yi Ding Ajay Puri Edward H M Wang Ashish Gulia Claire Durban Xiao-Hui Niu | 2015 | Chinese Medical Journal2015，，19： | 2 |
| 10 | Health and economic burden of the projected obesity trends in the USA and the UK显示文摘 | Y Claire Wang Klim McPherson Tim Marsh Steven L Gortmaker Martin Brown | 2011 | 2011 (9793)2011，，9793： | 1 |
| 11 | Rates of Adult Schizophrenia Following Prenatal exposure to the Chinese Famine of 1959-1961 显示文摘 | St Clair D Xu M Wang P | 2005 | JAMA2005，994，5： | 1 |
| 12 | Can local ecological knowledge be used to assess status and extinction drivers in a threatened freshwater cetacean?显示文摘 | Samuel T. Turvey Claire L. Risley Jeffrey E. Moore Leigh A. Barrett Hao Yujiang Zhao Xiujiang Zhou Kaiya Wang Ding | 2013 | Biological Conservation2013，，： | 1 |
| 13 | Rates of adult schizophrenia follow- ing prenatal exposure to the Chinese famine of 1959 - 1961 显示文摘 | St Clair D Xu M Wang P | 1959 | JA- MA1959，29，5： | 1 |
| 14 | Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959-1961显示文摘 | St Clair D Xu M Wang P | 2005 | JAMA2005，294，5： | 1 |
| 15 | Pharmacokinetic and Pharmacodynamic characteristics of emtricitabine support its once daily dosing for the treatment of HIV in fection显示文摘 | Wang LH Bcgley J St Claire RL | | 0，，11： | 1 |
| 16 | Pharmacokinetic and pharmacodynamic characteristics of emtricitabine support its once daily dosing for the treatment of HIV infection显示文摘 | Begley J St Claire RL | 2004 | AIDS ResHumRetroviruses2004，20，11： | 1 |
| 17 | PTEN and TNF-α regulation of the intestinal-specific Cdx-2 homeobox gene through a PI3K, PKB/Akt, and NF-κB–dependent pathway显示文摘 | Sunghoon Kim Claire Domon-Dell Qingding Wang Dai H. Chung Antonio Di Cristofano Pier Paolo Pandolfi Jean-Noel Freund B.Mark Evers | 2002 | Gastroenterology2002，，4： | 1 |
| 18 | miR-21 and miR-214 Are Consistently Modulated during Renal Injury in Rodent Models显示文摘 | Laura Denby Vasudev Ramdas Martin W. McBride Joe Wang Hollie Robinson John McClure Wendy Crawford Ruifang Lu Dianne Z. Hillyard Raya Khanin Reuven Agami Anna F. Dominiczak Claire C. Sharpe Andrew H. Baker | 2011 | The American Journal of Pathology2011，，2： | 1 |
| 19 | Clostridium absonum α-Toxin: New Insights into Clostridial Phospholipase C Substrate Binding and Specificity显示文摘 | Graeme C. Clark David C. Briggs Tadahiro Karasawa Xingmin Wang Ambrose R. Cole Tsuneo Maegawa Pramukh N. Jayasekera Claire E. Naylor Julie Miller David S. Moss Shinichi Nakamura Ajit K. Basak Richard W. Titball | 2003 | Journal of Molecular Biology2003，，4： | 1 |
| 20 | Trends and racial/ethnic disparities in severe obesity among US children and adolescents,1976-2006显示文摘 | Claire Wang Y Gortmaker SL Taveras EM | | 0，，01： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员