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    题名 作者 年代 出处 被引量
1Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics显示文摘交往受体的蛋白质 kinase-3 (RIP3 或 RIPK3 ) 是执行 “ 的细胞的机械的必要部分; programmed”或 “ regulated”坏死。这里,我们证明那规划坏死响应许多化学疗法的代理人被激活并且贡献导致化疗的房间死亡。然而,我们证明那 RIP3 表情经常在化学疗法的死亡期间由于它的 transcriptional 开始地点, MLKL 的这样 RIP3 依赖的激活和下游地规划的坏死附近的 genomic methylation 是在癌症房间的 silenced 大部分被镇压。不过,有 hypomethylating 代理人的治疗恢复 RIP3 表示,并且从而以一种 RIP3 依赖的方式把敏感提升到 chemotherapeutics。RIP3 表示在 85% 乳癌病人与正常织物相比在肿瘤被减少,建议那 RIP3 缺乏断然在肿瘤生长 / 发展期间被选择。因为 hypomethylating 代理人在病人是相当容忍得好的,我们建议病人们可以从收到 hypomethylating 代理人与常规 chemotherapeutics 在治疗以前导致 RIP3 表示有益于的那 RIP3 缺乏的癌症。Gi-Bang Koo Michael J Morgan Da-Gyum Lee Woo-Jung Kim Jung-Ho Yoon Ja Seung Koo Seung I1 Kim Soo Jung Kim Mi Kwon Son Soon Still Hong Jean M Mulcahy Levy Daniel A Pollyea Craig T Jordan Pearlly Yan David Frankhouser Deedra Nicolet Kati Maharry Guido Marcucci Kyeong Sook Choi Hyeseong Cho ndrew Thorbum You-Sun Kim 2015Cell Research2015,25,6:20
2Coordinated peak expression of MMP-26 and TIMP-4 in preinvasive human prostate tumor显示文摘因为早察觉和治疗为病人的医药管理是批评的,为早前列腺癌症诊断的新奇简历标记的鉴定是高度重要的。在基础房间层和地下室膜的连续性的混乱为高级职业人员静电干扰 intraepithelial 瘤形成(HGPIN ) 的前进是必要的到在人的前列腺的侵略腺癌。涉及变换到侵略显型的分子是强烈审查的题目。我们以前报导了矩阵 metalloproteinase-26 (MMP-26 ) 经由地下室膜蛋白质并且由激活 MMP-9 的酶原形式的劈开支持人的前列腺癌症房间的侵略。而且,我们发现了 metalloproteinases-4 (TIMP-4 ) 的那个织物禁止者是大多数有势力 MMP-26 的内长的禁止者。这里,我们更高示威(p<0.0001 ) 在 HGPIN 和癌症的 MMP-26 和 TIMP-4 表示,与非肿瘤的 acini 相比。他们的表示层次在 HGPIN 是最高的,但是在一样的纸巾在侵略癌症(为各个的 p<0.001 ) 衰退。连续前列腺癌症织物节染色的 Immunohistochemical 建议 MMP-26 和 TIMP-4 的 colocalization。现在的学习显示 MMP-26 和 TIMP-4 可以在 HGPIN 的变换期间起一个不可分的作用到侵略癌症并且可以也为早前列腺癌症诊断用作标记。房间研究(2006 ) 16:750-758。做 i:10.1038/sj .cr.7310089;出版联机 2006 年 8 月 29 日。Seakwoo Lee Kevin K Desai Kenneth A Iczkowski Robert G Newcomer Kevin J WU Yun-Ge Zhao Winston W Tan Mark D Roycik Qing-Xiang Amy Sang 2006Cell Research2006,16,9:18
3The wonders of BMP9:From mesenchymal stem cell differentiation,angiogenesis,neurogenesis,tumorigenesis,and metabolism to regenerative medicine显示文摘Although bone morphogenetic proteins(BMPs)initially showed effective induction of ectopic bone growth in muscle,it has since been determined that these proteins,as members of the TGF-b superfamily,play a diverse and critical array of biological roles.These roles include regulating skeletal and bone formation,angiogenesis,and development and homeostasis of multiple organ systems.Disruptions of the members of the TGF-b/BMP superfamily result in severe skeletal and extra-skeletal irregularities,suggesting high therapeutic potential from understanding this family of BMP proteins.Although it was once one of the least characterized BMPs,BMP9 has revealed itself to have the highest osteogenic potential across numerous experiments both in vitro and in vivo,with recent studies suggesting that the exceptional potency of BMP9 may result from unique signaling pathways that differentiate it from other BMPs.The effectiveness of BMP9 in inducing bone formation was recently revealed in promising experiments that demonstrated efficacy in the repair of critical sized cranial defects as well as compatibility with bone-inducing bio-implants,revealing the great translational promise of BMP9.Furthermore,emerging evidence indicates that,besides its osteogenic activity,BMP9 exerts a broad range of biological functions,including stem cell differentiation,angiogenesis,neurogenesis,tumorigenesis,and metabolism.This review aims to summarize our current understanding of BMP9 across biology and the body.Sami Mostafa Mikhail Pakvasa Elam Coalson Allen Zhu Alex Alverdy Hector Castillo Jiaming Fan Alex Li Yixiao Feng Di Wu Elliott Bishop Scott Du Mia Spezia Alissa Li Ofir Hagag Alison Deng Winny Liu Mingyang Li Sherwin S·Ho Aravind Athiviraham Michael J·Lee Jennifer Moriatis Wolf Guillermo A·Ameer Hue H·Luu Rex C·Haydon Jason Strelzow Kelly Hynes Tong-Chuan He Russell R·Reid 2019Genes & Diseases2019,6,3:15
4肌萎缩性侧索硬化蛋白激活小胶质细胞NLRP3炎性小体显示文摘小胶质细胞NLRP3炎性小体激活正在成为神经退行性变过程中神经炎症的关键因素。诸如β-淀粉样蛋白和α-突触核蛋白之类的致病性蛋白质聚集体触发小胶质NLRP3激活,从而导致半胱天冬酶-1激活和IL-1β的分泌。在小鼠肌萎缩性侧索硬化症(ALS)的SOD1G93A模型中,半胱天冬酶-1和IL-1β均促进疾病进展,提示小胶质NLRP3在该进程中发挥作用。然而先前的研究表明,SOD1G93A小鼠小胶质细胞不表达NLRP3,SOD1G93A蛋白在小胶质细胞中产生独立于NLRP3的IL-1β。本研究论证了使用Nlrp3-GFP基因敲入小鼠,在SOD1G93A小鼠中小胶质细胞表达NLRP3。本研究显示聚集和可溶性SOD1G93A均可激活小鼠原代小胶质细胞中的炎性小体,导致半胱天冬酶-1和IL-1β裂解,ASC斑点形成以及呈剂量和时间依赖性的IL-1β分泌。重要的是,SOD1G93A无法从缺乏Nlrp3的小胶质细胞或者用特异性NLRP3抑制剂MCC950预处理的小胶质细胞中诱导IL-1β分泌,从而证实NLRP3是介导SOD1诱导的小胶质细胞IL-1β分泌的关键炎症小体复合物。在TDP-43Q331K ALS小鼠模型中也观察到小胶质NLRP3上调,TDP-43野生型和突变蛋白亦可以NLRP3依赖性的方式激活小胶质炎性小体。从机制上讲,本研究确定了活性氧簇和ATP的生成是SOD1G93A介导的NLRP3激活所需的关键事件。总之,本研究的数据表明ALS小胶质细胞表达NLRP3,而病理ALS蛋白激活小胶质NLRP3炎性小体。因此,NLRP3抑制可能是阻止小胶质细胞神经炎症和ALS疾病进展的潜在治疗方法。Vandana Deora John D Lee Eduardo AAlbornoz Luke McAlary Cyril J Jagaraj Avril A B Robertson Julie D Atkin Matthew A Cooper Kate Schroder Justin J Yerbury Richard Gordon Trent MWoodruff 杜一星(编译) 2020神经损伤与功能重建2020,15,9:13
5Gastro-intestinal toxicity of chemotherapeutics in colorectal cancer:The role of inflammation显示文摘Chemotherapy-induced diarrhea(CID)is a common and often severe side effect experienced by colorectal cancer(CRC)patients during their treatment.As chemotherapy regimens evolve to include more efficacious agents,CID is increasingly becoming a major cause of dose limiting toxicity and merits further investigation.Inflammation is a key factor behind gastrointestinal(GI)toxicity of chemotherapy.Different chemotherapeutic agents activate a diverse range of pro-inflammatory pathways culminating in distinct histopathological changes in the small intestine and colonic mucosa.Here we review the current understanding of the mechanisms behind GI toxicity and the mucositis associated with systemic treatment of CRC.Insights into the inflammatory response activated during this process gained from various models of GI toxicity are discussed.The inflammatory processes contributing to the GI toxicity of chemotherapeutic agents are increasingly being recognised as having an important role in the development of anti-tumor immunity,thus conferring added benefit against tumor recurrence and improving patient survival.We review the basic mechanisms involved in the promotion of immunogenic cell death and its relevance in the treatment of colorectal cancer.Finally,the impact of CID on patient outcomes and therapeutic strategies to prevent or minimise the effect of GI toxicity and mucositis are discussed.Chun Seng Lee Elizabeth J Ryan Glen A Doherty 2014World Journal of Gastroenterology2014,20,14:10
6CD69 expression on airway eosinophils and airway inflammation in a murine model of asthma显示文摘Background Asthma is a chronic airway disease with inflammation characterized by physiological changes (airway hyper-responsiveness, AHR) and pathological changes (inflammatory cells infiltration and mucus production). Eosinophils play a key role in the allergic inflammation. But the causative relationship between eosinophils and airway inflammation is hard to prove. One of the reasons is lack of activation marker of murine eosinophils. We investigated the expression of CD69 on murine eosinophils in vitro, the relationship between the expression of CD69 on eosinophils from peripheral blood and bronchoalveolar lavage fluid and on airway inflammation in asthmatic mice. Methods Eosinophils from peripheral blood of IL-5 transgenic mice (NJ.1638) were purified. Mice were divided into five groups: wild type mice sensitized and challenged with saline (WS group), wild type mice sensitized and challenged with ovalbumin (WO group), IL-5-/- mice sensitized and challenged with saline and transferred with purified eosinophils (ISE group), IL-5-/- mice sensitized and challenged with OVA and transferred with purified eosinophils (IOE group), IL-5-/- mice sensitized and challenged with OVA and transferred with purified eosinophils, pretreated with anti CD4 monoclonal antibody (IOE+antiCD4mAb group). IL-5-/- mice were sensitized with OVA at day 0 and day 14, then challenged with OVA aerosol. On days 24, 25, 26 and 27 purified eosinophils were transferred intratracheally to IL-5-/- mice. On day 28, blood and BALF were collected and CD69 expression on eosinophils measured by flowcytometry. Results Purified eosinophils did not express CD69. But eosinophils cultured with PMA+MA, IFN-γ, IL-5 or GM-CSF expressed CD69 strongly. Eosinophils from blood of WO, WS group did not express CD69 at all. The numbers of eosinophils in BALF of WO group, IOE group, ISE group and IOE+antiCD4mAb group were significantly higher than in mice of WS group which did not have eosinophils at all. CD69 expression on eosinophils in BALF of IOE and WO groups was strong. Eosinophils in BALF of ISE and IOE+antiCDmAb groups did not express CD69. The mucus production result was similar to CD69 expression. There were eosinophils infiltration in lung slides of all groups except WS group. Conclusion Activation in airway of eosinophils could directly lead to airway inflammation.WANG Hui-ying SHEN Hua-hao James J Lee Nancy A Lee 2006Chinese Medical Journal2006,,23:8
7Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart显示文摘出生后的心通过 hypertrophic 生长适应应力和超载,可能病理学或有益的一个过程(生理的肥大) 。生理的肥大改进心脏的性能在健康并且 diseased 个人,然而,宣传这有利改编的机制仍然保持糟糕定义。我们识别 cytokine cardiotrophin (CT1 ) 1 作为能够包括导致的导出 cardiomyocyte 的 angiogenic 信号的心肌层,和刺激的短暂、可逆的肥大概括心的生理的生长的特色的一个因素增加了由脉管形成。CT1 的能力从 caspase 激活的调停 CK2 的制止发源导致生理的肥大,阻止到无限制的病理学的生长的转变。外长的 CT1 蛋白质交货稀释了病理并且在正确的心失败的一个严格的模型恢复了可收缩的功能,建议为这难处理的心脏病的一种新奇处理选择。Mohammad Abdul-Ghani Colin Suen Baohua Jiang Yupu Deng Jonathan J Weldrick Charis Putinski Steve Brunette Pasan Femando Tom T Lee Peter Flynn Frans H H Leenen Patrick G Burgon Duncan J Stewar Lynn A Megeney 2017Cell Research2017,27,10:8
8如何设计高质量针刺临床研究:基于证据的专家共识显示文摘本针刺随机对照试验(Randomised controlled trials, RCT)专家共识是基于目前针刺试验面临的最普遍、最关键问题,由临床医生、研究人员、从事针灸和外科的临床试验专家、统计专家、临床流行病学和方法学专家以及患者组成的国际临床研究小组联合制订。该共识将有助于临床试验资助者、注册者以及期刊编辑等评估针刺RCT方案及研究结果的相关性、重要性和质量。张誉清 焦睿珉 Claudia M Witt 劳力行 刘建平 Lehana Thabane Karen J Sherman Mike Cummings Dawn P Richards Eun-Kyung Anna Kim Tae-Hun Kim Myeong Soo Lee Michael E Wechsler Benno Brinkhaus Jun J Mao Caroline A Smith 岗卫娟 刘保延 刘志顺 刘岩 郑晖 吴佳霓 AloBSO Carrasco-Labra Mohit Bhandari Philip J Devereaux 景向红 Gordon Guyatt 2022英国医学杂志中文版2022,25,6:7
9CD69的表达在小鼠嗜酸细胞的活化与凋亡中的作用显示文摘目的:观察在体内、体外不同条件下小鼠嗜酸细胞(EOS)表面CD69的表达与细胞存活率,探讨CD69的表达在小鼠EOS的活化、凋亡中的作用。方法:提纯IL-5高分泌转基因小鼠外周血中的EOS,测定其表面CD69的表达,体外以PMA+MA刺激EOS,在1 h、12 h、18 h、24 h测定细胞表面CD69的表达与细胞存活率;分别以1μg/L的IL-4、IL-5、IL-12、IL-13、IFN-γ、GM-CSF培养EOS18 h后测定细胞的存活率与表面CD69的表达。制备小鼠哮喘模型,观察CD69在小鼠BALF、外周血EOS中的表达。结果:新鲜提纯的小鼠外周血EOS不表达CD69,PMA+MA刺激的EOS在1 h后即有CD69的表达,12 h表达至高峰,至少持续24 h以上;但细胞的存活率快速下降。不同细胞因子对EOS的培养均可诱导CD69的表达,其中IL-13、IFN-γ、GM-CSF对此影响明显,且GM-CSF可显著抑制EOS的凋亡;哮喘小鼠外周血EOS无CD69的表达,而BALF中EOS可有CD69的表达。结论:静止小鼠EOS表面不表达CD69,但在体内、体外不同条件下激活的EOS表面均有CD69的表达;同时,体外实验显示CD69的表达与细胞凋亡密切相关。结果提示CD69既可作为EOS激活的表面标记物,同时又可诱导EOS的凋亡,这为哮喘治疗提供新的思路。汪慧英 James J Lee Nancy A Lee 2009中国病理生理杂志2009,25,1:7
10Murine lung eosinophil activation and chemokine production in allergic airway inflammation显示文摘Eosinophils play important roles in asthma and lung infections.Murine models are widely used for assessing the functional significance and mechanistic basis for eosinophil involvements in these diseases.However,little is known about tissue eosinophils in homeostasis.In addition,little data on eosinophil chemokine production during allergic airway inflammation are available.In this study,the properties and functions of homeostatic and activated eosinophils were compared.Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1,B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex(MHC)class II,and were found to be poor stimulators of T-cell proliferation.However,these eosinophils expressed high levels of chemokine mRNA including C10,macrophage inflammatory protein(MIP)-1a,MIP-1c,MIP-2,eotaxin and monocyte chemoattractant protein-5(MCP-5),and produced chemokine proteins.Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation.Lung eosinophils from mice with induced allergic airway inflammation exhibited increased chemokines mRNA expression and chemokines protein production and upregulated MHC class II and CD11c expression.They were also found to be the predominant producers of the CCR1 ligands CCL6/C10 and CCL9/MIP-1c in inflamed lungs.Eosinophil production of C10 and MIP-1c correlated with the marked influx of CD11bhigh lung dendritic cells during allergic airway inflammation and the high expression of CCR1 on these dendritic cells(DCs).The study provided baseline information on tissue eosinophils,documented the upregulation of activation markers and chemokine production in activated eosinophils,and indicated that eosinophils were a key chemokine-producing cell type in allergic lung inflammation.C Edward Rose Jr Joanne A Lannigan Paul Kim James J Lee Shu Man Fu Sun-sang J Sung 2010Cellular & Molecular Immunology2010,7,5:6
11Clinical outcomes following salvage Gamma Knife radiosurgery for recurrent glioblastoma显示文摘Glioblastoma multiforme(GBM) is the most common malignant primary brain tumor with a survival prognosis of 14-16 mo for the highest functioning patients. Despite aggressive, multimodal upfront therapies, the majority of GBMs will recur in approximately six months. Salvage therapy options for recurrent GBM(r GBM) are an area of intense research. This study compares recent survival and quality of life outcomes following Gamma Knife radiosurgery(GKRS) salvage therapy. Following a Pub Med search for studies usingGKRS as salvage therapy for malignant gliomas, nine articles from 2005 to July 2013 were identified which evaluated rG BM treatment. In this review, we compare overall survival following diagnosis, overall survival following salvage treatment, progression-free survival, time to recurrence, local tumor control, and adverse radiation effects. This report discusses results for rG BM patient populations alone, not for mixed populations with other tumor histology grades. All nine studies reported median overall survival rates(from diagnosis, range:16.7-33.2 mo; from salvage, range:9-17.9 mo). Three studies identified median progression-free survival(range:4.6-14.9 mo). Two showed median time to recurrence of GBM. Two discussed local tumor control. Six studies reported adverse radiation effects(range:0%-46% of patients). The greatest survival advantages were seen in patients who received GKRS salvage along with other treatments, like resection or bevacizumab, suggesting that appropriately tailored multimodal therapy should be considered with each rG BM patient. However, there needs to be a randomized clinical trial to test GKRS for rG BM before the possibility of selection bias can be dismissed.Erik W Larson Halloran E Peterson Wayne T Lamoreaux Alexander R MacKay Robert K Fairbanks Jason A Call Jonathan D Carlson Benjamin C Ling John J Demakas Barton S Cooke Christopher M Lee 2014World Journal of Clinical Oncology2014,5,2:5
12Fatigue behavior of high-entropy alloys: A review显示文摘Fatigue failures cost approximately 4% of the United States' gross domestic product(GDP). The design of highly fatigue-resistant materials is always in demand. Different from conventional strategies of alloy design, high-entropy alloys(HEAs) are defined as materials with five or more principal elements, which could be solid solutions. This locally-disordered structure is expected to lead to unique fatigue-resistant properties. In this review, the studies of the fatigue behavior of HEAs during the last five years are summarized. The four-point-bending high-cycle fatigue coupled with statistical modelling, and the fatigue-crack-growth behavior of HEAs, are reviewed. The effects of sample defects and nanotwins-deformation mechanisms on four-point-bending high-cycle fatigue of HEAs are discussed in detail. The influence of stress ratio and temperature on fatigue-crack-growth characteristics of HEAs is also discussed. HEAs could exhibit comparable or greater fatigue properties, relative to conventional materials. Finally,the possible future work regarding the fatigue behavior of HEAs is suggested.CHEN PeiYong LEE Chanho WANG Shao-Yu SEIFI Mohsen LEWANDOWSKI John J DAHMEN Karin A JIA HaoLing XIE Xie CHEN BiLin YEH Jien-Wei TSAI Che-Wei YUAN Tao LIAW Peter K 2018Science China(Technological Sciences)2018,61,2:3
13Prognostic impact of the Bismuth-Corlette classification:Higher rates of local unresectability in stageⅢb hilar cholangiocarcinoma显示文摘Background:The Bismuth-Corlette(BC)classification is used to categorize hilar cholangiocarcinoma by proximal extension along the biliary tree.As the right hepatic artery crosses just behind the left bile duct,we hypothesized that BCⅢb tumors would have a higher likelihood of local unresectability due to involvement of the contralateral artery.Methods:A retrospective review of a prospectively maintained database identified patients with hilar cholangiocarcinoma taken to the operating room for intended curative resection between April 2008 and September 2016.Cases were assigned BC stages based on preoperative imaging.Results:Sixty-eight patients were included in the study.All underwent staging laparoscopy after which 16 cases were aborted for metastatic disease.Of the remaining 52 cases,14 cases were explored and aborted for locally advanced disease.Thirty-eight underwent attempt at curative resection.After exclud-ing cases aborted for metastatic disease,the chance of proceeding with resection was 55.6%for BCⅢb staged lesions compared to 80.0%of BCⅢa lesions and to 82.4%for BCⅠ-Ⅲa staged lesions(P<0.05).About 44.4%of BCⅢb lesions were aborted for locally advanced disease versus 17.6%of remaining BC stages.Conclusions:When hilar cholangiocarcinoma is preoperatively staged as BCⅢb,surgeons should antici-pate higher rates of locally unresectable disease,likely involving the right hepatic artery.Michael J Passeri Maria R Baimas-George Jesse K Sulzer David A Iannitti John B Martinie Erin H Baker Lee M Ocuin Dionisios Vrochides 2020Hepatobiliary & Pancreatic Diseases International2020,19,2:3
14How often are angiotentensin Ⅱ and aldosterrone concentrations raised during chronic ACEinhibitortreatment in cardiacfailure显示文摘MAC FADYEN R J LEE A F MORTON J J 1999Heart1999,82,1:2
15The extent of algal and bacterial endosymbioses in protozoa显示文摘Lee J J Soldo A N Reisser W 1985J Protozool1985,32,3:2
16Drugs Associated with Hepatotoxicity and their Reporting Frequency of Liver Adverse Events in VigiBase(TM)显示文摘Suzuki Ayako Andrade Raul J Bjornsson Einar Lucena M Isabel Lee William M Yuen Nancy A Hunt Christine M Freston James W 2010Drug Safety2010,,6:2
17SLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueduct显示文摘Pendred syndrome(PS) is characterized by autosomal recessive inheritance of goiter associated with a defect of iodide organification, hearing loss, enlargement of the vestibular aqueduct(EVA), and mutations of the SLC26A4 gene. However, not all EVA patients have PSor SLC26A4 mutations. Two mutant alleles of SLC26A4 are detected in 1/4 of North American or European EVA populations, one mutant allele is detected in another 1/4 of patient populations, and no mutations are detected in the other 1/2. The presence of two mutant alleles of SLC26A4 is associated with abnormal iodide organification, increased thyroid gland volume, increased severity of hearing loss, and bilateral EVA. The presence of a single mutant allele of SLC26A4 is associated with normal iodide organification, normal thyroid gland volume, less severe hearing loss and either bilateral or unilateral EVA. When other underlying correlations are accounted for, the presence of a cochlear malformation or the size of EVA does not have an effect on hearing thresholds. This is consistent with observations of an Slc26a4 mutant mouse model of EVA in which hearing loss is independent of endolymphatic hydrops or inner ear malformations. Segregation analyses of EVA in families suggest that the patients carrying one mutant allele of SLC26A4 have a second, undetected mutant allele of SLC26A4, and the probability of a sibling having EVA is consistent with its segregation as an autosomal recessive trait. Patients without any mutations are an etiologically heterogeneous group in which siblings have a lower probability of having EVA. SLC26A4 mutation testing can provide prognostic information to guide clinical surveillance and management, as well as the probability of EVA affecting a sibling.Taku Ito Julie Muskett Parna Chattaraj Byung Yoon Choi Kyu Yup Lee Christopher K Zalewski Kelly A King Xiangming Li Philine Wangemann Thomas Shawker Carmen C Brewer Seth L Alper Andrew J Griffith 2013World Journal of Otorhinolaryngology2013,3,2:2
18卒中介入治疗培训指南:国际多学会共识文件显示文摘1背景 缺血性卒中是全球人口死亡和残疾的首要原因。很多急性大血管闭塞(emergent large vesselocclusion,ELVO)患者都会遗留长期残疾。事实上,这些颅内大动脉闭塞经常会导致大面积脑损伤,进而造成患者死亡或严重致残。Lavine SD Cockroft K Hoh B Bambakidis N Khalessi AA Woo H Riina H Siddiqui A Hirsch JA Chong W Rice H Wenderoth J Mitchell P Coulthard A Signh TJ Phatorous C Khangure M Klurfan P ter Brugge K Iancu D Gunnarsson T Pongpech S Rodesch G Soderman M Taylor A Krings T Orbach D Picard L Suh DC Zheng HQ Jansen O Muto M Szikora I Pierot L Brouwer P Gralla J Renowden S Andersson T Fiehler J Turjman F White P Januel AC Spelle L Kulcsar Z Chapot R Biondi A Dima S Taschner C Szajner M Krajina A Sakai N Matsumaru Y Yoshknura S Ezura M Fujinaka T Iihara K Ishii A Higashi T Hirohata M Hyodo A Ito Y Kawanishi M Kiyosue H Kobayashi E Kobayashi S Kuwayama N Matsumoto Y Miyachi S Murayama Y Nagata I Nakahara I Nemoto S Niimi Y Oishi H Satomi J Satow T Sugiu K Tanaka M Terada T Yamagami H Diaz O Lylyk P Jayaraman MV Patsalides A Gandhi CD Lee SK Abruzzo T Albani B Ansari SA Arthur AS Baxter BW Bulsara KR Chen M Almandoz JE Fraser JF Heck DV Hetts SW Hussain MS Klucznik RP Leslie-Mawzi TM Mack WJ McTaggart RA Meyers PM Mocco J Prestigiacomo CA Pride GL Rasmussen PA Starke RM Sunenshine PJ Tarr RW Frei DF Pabo M Nogueira RG Zaidat OO Jovin T Linfante I Yavagal D Liebeskind D Novakovic R Pongpech S 许岩 孙瑞 郭芮兵 2017国际脑血管病杂志2017,25,5:2
19Enzyme-linked Immunosorbent Assays for the Insecticide Fenitrothion Influence of Hapten Conformation and Sample Matrix on Assay Performance 显示文摘KIM Y J KIM Y A LEE Y T 2007Analytica Chimica Acta2007,591,:1
20Identification of three genetic loci controlling leaf senescence in Arabidopsis thaliana显示文摘OH S A PARK J H LEE G I PACK K H PARK S K NAM H G 1997Plant Journal1997,12,3:1
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