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1Evolving concepts in bone infection: redefining “biofilm”,“acute vs. chronic osteomyelitis”, “the immune proteome” and “local antibiotic therapy”显示文摘Osteomyelitis is a devastating disease caused by microbial infection of bone. While the frequency of infection following elective orthopedic surgery is low, rates of reinfection are disturbingly high. Staphylococcus aureus is responsible for the majority of chronic osteomyelitis cases and is often considered to be incurable due to bacterial persistence deep within bone. Unfortunately, there is no consensus on clinical classifications of osteomyelitis and the ensuing treatment algorithm. Given the high patient morbidity,mortality, and economic burden caused by osteomyelitis, it is important to elucidate mechanisms of bone infection to inform novel strategies for prevention and curative treatment. Recent discoveries in this field have identified three distinct reservoirs of bacterial biofilm including: Staphylococcal abscess communities in the local soft tissue and bone marrow, glycocalyx formation on implant hardware and necrotic tissue, and colonization of the osteocyte-lacuno canalicular network(OLCN) of cortical bone. In contrast, S.aureus intracellular persistence in bone cells has not been substantiated in vivo, which challenges this mode of chronic osteomyelitis. There have also been major advances in our understanding of the immune proteome against S. aureus, from clinical studies of serum antibodies and media enriched for newly synthesized antibodies(MENSA), which may provide new opportunities for osteomyelitis diagnosis, prognosis, and vaccine development. Finally, novel therapies such as antimicrobial implant coatings and antibiotic impregnated 3D-printed scaffolds represent promising strategies for preventing and managing this devastating disease. Here, we review these recent advances and highlight translational opportunities towards a cure.Elysia A. Masters Ryan P. Trombetta Karen L. de Mesy Bentley Brendan F Boyce Ann Lindley Gill Steven R. Gill Kohei Nishitani Masahiro Ishikawa Yugo Morita Hiromu Ito Sheila N. Bello-Irizarry Mark Ninomiya James D. Brodell Jr. Charles C. Lee Stephanie P. Hao Irvin Oh Chao Xie Hani A. Awad John L. Daiss John R. Owen Stephen L. Kates Edward M. Schwarz Gowrishankar Muthukrishnan 2019Bone Research2019,7,3:19
2Neuroprotective mechanisms and translational potential of therapeutic hypothermia in the treatment of ischemic stroke显示文摘Stroke is a leading cause of disability and death,yet effective treatments for acute stroke has been very limited.Thus far,tissue plasminogen activator has been the only FDA-approved drug for thrombolytic treatment of ischemic stroke patients,yet its application is only applicable to less than 4–5% of stroke patients due to the narrow therapeutic window(< 4.5 hours after the onset of stroke) and the high risk of hemorrhagic transformation.Emerging evidence from basic and clinical studies has shown that therapeutic hypothermia,also known as targeted temperature management,can be a promising therapy for patients with different types of stroke.Moreover,the success in animal models using pharmacologically induced hypothermia(PIH) has gained increasing momentum for clinical translation of hypothermic therapy.This review provides an updated overview of the mechanisms and protective effects of therapeutic hypothermia,as well as the recent development and findings behind PIH treatment.It is expected that a safe and effective hypothermic therapy has a high translational potential for clinical treatment of patients with stroke and other CNS injuries.Jin Hwan Lee James Zhang Shan Ping Yu 2017Neural Regeneration Research2017,12,3:19
3计算机辅助模型外科设计及虚拟板的临床应用显示文摘目的:通过计算机辅助软件进行正颌手术模型外科设计,经快速原型技术制作板,探讨该板的临床应用价值。方法:15例颌面畸形需要正颌手术的患者均进行全头颅三维CT扫描(层厚0.625mm),将DICOM格式的CT数据输入电脑软件Simplant CMF(Materialise Medical,Leuven,Belgium)。通过软件对头颅模型进行上下颌骨的分离、截骨线的设计、截骨、骨块移动等操作,收集并输出数据,经快速原型机制作板(虚拟板)。同时,每例患者还进行传统石膏模型外科以及传统板制作。术中首先利用虚拟板进行骨块的移动和固定,然后应用传统板检验骨块的新位置,验证虚拟板的临床实用性。结果:15例患者中,4例单颌手术(双侧下颌支矢状劈开术)、10例双颌手术(Le Fort I型整体截骨术+双侧下颌支矢状劈开术)以及1例双颌手术(Le Fort I型分块截骨术+双侧下颌支矢状劈开术)。手术中,12例患者的虚拟板完全符合临床要求。3例患者(包括1例双侧下颌支矢状劈开术和2例Le Fort I型整体截骨术+双侧下颌支矢状劈开术)的虚拟板与传统板之间有部分偏差,遂通过传统板进行骨块的重新固定。结论:计算机辅助设计可完成Le Fort I型整体(或分块)截骨术和双侧下颌支矢状劈开术的模型外科,虚拟板基本可实现传统板的功能。通过对软件的进一步熟悉、更多病例的积累,计算机辅助模型外科可能取代传统的石膏模型外科。王旭东 Philip KM Lee 沈国芳 房兵 吴勇 蔡鸣 James Chow 2008中国口腔颌面外科杂志2008,6,6:16
4Portal hypertension: Imaging of portosystemic collateral pathways and associated image-guided therapy显示文摘Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen. A brief overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.Murad Feroz Bandali Anirudh Mirakhur Edward Wolfgang Lee Mollie Clarke Ferris David James Sadler Robin Ritchie Gray Jason Kam Wong 2017World Journal of Gastroenterology2017,23,10:14
5Calcium signaling and T-type calcium channels in cancer cell cycling显示文摘Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca2+ channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca2+ channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel isminimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca2+ channels are not expressed in epithelial cells, selective T-type Ca2+ channel blockers may be useful in the treatment of certain types of cancers.James T Taylor Xiang-Bin Zeng Jonathan E Pottle Kevin Lee Alun R Wang Stephenie G Yi lennifer A S Scruggs Suresh S Sikka Ming Li 2008World Journal of Gastroenterology2008,14,32:12
6Full-color micro-LED display with high color stability using semipolar(20-21) InGaN LEDs and quantum-dot photoresist显示文摘Red-green-blue(RGB)full-color micro light-emitting diodes(μ-LEDs)fabricated from semipolar(20-21)wafers,with a quantum-dot photoresist color-conversion layer,were demonstrated.The semipolar(20-21)In Ga N/Ga Nμ-LEDs were fabricated on large(4 in.)patterned sapphire substrates by orientation-controlled epitaxy.The semipolarμ-LEDs showed a 3.2 nm peak wavelength shift and a 14.7%efficiency droop under 200 A∕cm2injected current density,indicating significant amelioration of the quantum-confined Stark effect.Because of the semipolarμ-LEDs’emission-wavelength stability,the RGB pixel showed little color shift with current density and achieved a wide color gamut(114.4%NTSC space and 85.4%Rec.2020).SUNG-WEN HUANG CHEN YU-MING HUANG KONTHOUJAM JAMES SINGH YU-CHIEN HSU FANG-JYUN LIOU JIE SONG JOOWON CHOI PO-TSUNG LEE CHIEN-CHUNG LIN ZHONG CHEN JUNG HAN TINGZHU WU HAO-CHUNG KUO 2020Photonics Research2020,8,5:12
7A truncated hepatitis E virus ORF2 protein expressed in tobacco plastids is immunogenic in mice显示文摘瞄准:表示 23-ku pE2 到花费有效地,肝炎 E 病毒(HEV ) 的 3'-portion 包括的 E2 碎片编码的最有希望的子单元疫苗打开读物框架 2 (ORF2 ) 在烟草的质体(Nicotiana 烟 cv。SR1 ) ,在质体调查 transgene 表示和 pE2 累积,并且评估反在老鼠的导出质体的 pE2 的遗传因子的效果。方法:包含米饭 psbA 倡导者驾驶的 E2 碎片的指向质体的向量 pRB94-E2 被构造。在进烟草质体的交货之上,这构造能在质体染色体在 psaB-trnfM 和 trnG-psbC 碎片开始相应再结合,并且导致在二碎片之间插入的 transgene。pRB94-E2 与一个 biolistic 粒子轰炸方法被交付,并且转变质体的工厂被获得在补充 spectinomycin 的媒介上跟随炮轰的叶纸巾的新生。改革工厂的 Transplastomic 地位被 PCR 和南部的污点分析证实, transgene 表示被北污点分析调查,并且 pE2 的累积被 ELISA 测量。而且,蛋白浸出物被用来使老鼠免疫,并且在使免疫的老鼠的浆液样品的 pE2 反应的抗体的存在被 ELISA 学习。结果:PCR 和南部的污点分析证实的 Transplastomic 线能活跃地抄录 E2 mRNA。pE2 多肽象 13.27 microg/g 一样高被积累到水平新鲜叶子。pE2 能刺激使免疫的老鼠产生 pE2 特定的抗体。结论:HEV-E2 碎片能被插入到质体染色体,导出的 recombinant pE2 抗原是在老鼠遗传因子的反。因此,质体可以是为 HEV 疫苗的划算的生产的新奇来源。Yuan-Xiang Zhou Maggie Yuk-Ting Lee James Ming-Him Ng Mee-Len Chye Wing-Kin Yip Sze-Yong Zee Eric Lam 2006World Journal of Gastroenterology2006,12,2:10
8CD69 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
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
11Robot-Assisted Minimally Invasive Distal Pancreatectomy Is Superior to the Laparoscopic Technique显示文摘Mustapha Daouadi Amer H. Zureikat Mazen S. Zenati Haroon Choudry Alan Tsung David L. Bartlett Steven J. Hughes Ken K. Lee A. James Moser Herbert J. Zeh 2013Annals of Surgery2013,,1:6
12Dynamic chromatin states in human ES cells reveal potential regulatory sequences and genes involved in pluripotency显示文摘Pluripotency,一个细胞的能力区分并且产生所有胚胎的系,定义象胚胎的茎(ES ) 那样的哺乳动物的细胞类型的一个小数字细胞。当它通常被保持了时,那 pluripotency 是 transcriptional 的产品激活并且维持关键干细胞基因的表达式的规章的网络,积累的证据在建立并且保卫 ES 房间的 pluripotency 为 epigenetic 进程正在指向一个关键角色,象维持区分的房间类型的身份一样。以便更好在 pluripotency 理解 epigenetic 机制的角色,我们检验了在经历区别进一个 mesendodermal 系的人的 ES 房间(hESCs ) 染色体宽的染色质修正的动力学。我们发现在倡导者的染色质修正在区别期间仍然保持大部分不变,除了在在在 H3K27 的 acetylation 和 methylation 之间的一个动态开关标记在基因表示的激活和 silencing 之间的转变的倡导者的一个小数字,建议在在大多数差别上的房间命运承诺的一个层次表示了基因。我们也在 50 000 潜在的 enhancers 上印射,并且在染色质修正,特别 H3K4me1 和 H3K27ac 观察了大得多的动力学,它与他们的潜在的目标基因的表示相关。这些 enhancers 的进一步的分析揭示了 pluripotency 和可以在 hESCs 授与发展胜任的一个平衡状态的一口染色质签名陈述语气的潜在地关键的 transcriptional 管理者。我们的结果提供在定义 enhancers 和 pluripotency 支持染色质修正的角色的新证据。R David Hawkins Gary C Hon Chuhu Yang Jessica E Antosiewicz-Bourget Leonard K Lee Que-Minh Ngo Sarit Klugman Keith A Ching Lee E Edsall Zhen Ye Samantha Kuan Pengzhi Yu Hui Liu Xinmin Zhang Roland D Green Victor V Lobanenkov Ron Stewart James A Thomson Bing Ren 2011Cell Research2011,21,10:6
13Eosinophil-derived CCL-6 impairs hematopoietic stem cell homeostasis显示文摘嗜曙红血球(曙光女神) 长在层次造血的系统被看作了结束阶段受动器房间。证据的众多的线建议了那个曙光女神是关于各种各样的煽动性或有免疫力的反应的开始,繁殖和规定的多功能的白血球,特别在过敏疾病。最近的研究证明了那个曙光女神也为骨头髓血浆房间的维护和 B 房间的区别被要求。然而,曙光女神是否贡献造血的干细胞(HSC ) 的规定,仍然保持不清楚动态平衡。这里,我们证明曙光女神由在野类型的老鼠损害 HSC 静止和体质能力破坏 HSC 动态平衡后面的 ovalbumin (卵) 挑战并且甚至由引起骨头髓 HSC 在 Cd3-Il-5 转基因的老鼠的失败和疲劳。HSC 的损害维护和功能与导致曙光女神的氧化还原作用不平衡(增加的氧化 phosphorylation 和减少的抗氧化剂层次) 被联系。用集体 spectrometry,更重要地,我们决定 CCL-6 在嗜曙红血球过多下面在高水平被表示。我们证明 CCL-6 为损害 HSC 动态平衡导出曙光女神、负责。有趣地,有特定的抵销抗体的 CCL-6 的阻塞,当在质问卵的老鼠加重嗜曙红血球过多航线发炎时,恢复了 HSC 的体质能力。因此,我们的学习在 HSC 动态平衡揭示 Eos/CCL-6 的意外功能。Chao Zhang, Fei Li, Xufei Du, Man Luo, Wen Hua, Wen Li, Zhihua Chen, Songmin Ying, Huahao Shen Weiwei Yi, Hu Wang, Zhenyu Ju Hu Wang, Zhenyu Ju Ping Wu, Chao Peng, Catherine CL Wong James J Lee Songmin Ying Songmin Ying Huahao Shen 2018Cell Research2018,28,3:6
14Patterns of in-hospital mortality and bleeding complications following PCI for very elderly patients: insights from the Dartmouth Dynamic Registry显示文摘BackgroundVery 老病人(年龄 85 年) 是人口的一个很快增加的片断。作为一个组,他们经历跟随经皮的冠的干预(一种总线标准) 的在里面医院死亡和流血复杂并发症的高率。然而,在流血和死亡在之间的关系老 unknown.MethodsRetrospective 评论在 Dartmouth-Hitchcock 从 2000 ~ 2015 在 17,378 连续一种总线标准过程上被执行医学中心。在索引一种总线标准承认期间流血的发生(流血要求的输送,存取地点 hematoma > 5 厘米, pseudoaneurysm,和 retroperitoneal 流血)? 并且在里面医院死亡为四个年龄组被报导(< 65 年, 65-74 年, 75-84 年,和 85 年) 。承受了谁的流血复杂并发症和那些的病人的死亡被计算, multivariate 分析为在里面医院被执行死亡。最后,知道流血的预言者在病人年龄之间被比较 < 85 年和年龄 17,378 个病人学习了的 85 years.ResultsOf,(5.9%) 1019 经历了流血,(2.1%) 369 死了在里面医院追随者一种总线标准。流血和在里面医院死亡的发生与增加年龄 monotonically 增加了(死亡:0.94% , 2.27% , 4.24% 和 4.58% ;流血:3.96% , 6.62% , 10.68% 和 13.99% 好久 < 65, 65-74, 75-84 和 85 年,分别地) 。除了病人年龄 85 年,在 multivariate 分析上,流血为所有年龄组与增加的死亡被联系[机会比率(95% CI ) :变老 < 65 年, 3.65 (1.99-6.74 ) ;年龄 65-74 年, 2.83 (1.62-4.94 ) ;年龄 75-84 年, 3.86 (2.56-5.82 ) ,年龄 85 年:1.39 (0.49-3.95 )] 有增加的 .ConclusionsBleeding 和死亡追随者一种总线标准增加变老。为老尽管有流血的高率,流血在里面医院死亡追随者一种总线标准不再是预兆的。Shawn X Li Hannah I Chaudry Jiyong Lee Theodore B Curran Vishesh Kumar Kendrew K Wong Bruce W Andrus James T DeVries 2018Journal of Geriatric Cardiology2018,15,2:6
15Hepatic lipid homeostasis by peroxisome proliferator-activated receptor gamma 2显示文摘Peroxisome proliferator-activated receptor gamma(PPARγor PPARG)is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily.It plays a master role in the differentiation and proliferation of adipose tissues.It has two major isoforms,PPARγ1 and PPARγ2,encoded from a single gene using two separate promoters and alternative splicing.Among them,PPARγ2 is most abundantly expressed in adipocytes and plays major adipogenic and lipogenic roles in the tissue.Furthermore,it has been shown that PPARγ2 is also expressed in the liver,specifically in hepatocytes,and its expression level positively correlates with fat accumulation induced by pathological conditions such as obesity and diabetes.Knockout of the hepatic Pparg gene ameliorates hepatic steatosis induced by diet or genetic manipulations.Transcriptional activation of Pparg in the liver induces the adipogenic program to store fatty acids in lipid droplets as observed in adipocytes.Understanding how the hepatic Pparg gene expression is regulated will help develop preventative and therapeutic treatments for non-alcoholic fatty liver disease(NAFLD).Due to the potential adverse effect of hepatic Pparg gene deletion on peripheral tissue functions,therapeutic interventions that target PPAR g for fatty liver diseases require fine-tuning of this gene's expression and transcriptional activity。Yoon Kwang Lee Jung Eun Park Mikang Lee James P.Hardwick 2018Liver Research2018,2,4:5
16Risk factors for post-ERCP pancreatitis: A prospective, multicenter study显示文摘Martin L. Freeman James A. DiSario Douglas B. Nelson M.Brian Fennerty John G. Lee David J. Bjorkman Carol S. Overby Johannes Aas Michael E. Ryan Gary S. Bochna Michael J. Shaw Harry W. Snady Robert V. Erickson Joseph P. Moore Joseph P. Roel 2001Gastrointestinal Endoscopy2001,,4:5
17Tumor 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 2004Journal of Microbiology and Immunology2004,2,4:5
18元明清时期中国西南地区的交通发展显示文摘元明清时期,中国西南地区主要存在6条对外通道,虽然各条道路的旅行时间在这一时期变化不大,但元明清政府所投入的巨大人力物力极大地改善了西南水陆交通状况,降低了交通运输成本,使西南地区的贸易量有了显著的增长。 林文勋 秦树才(译) 2008思想战线2008,34,2:5
19RFP-mediated ubiquitination of PTEN modulates its effect on AKT activation显示文摘PTEN 肿瘤 suppressor 是在调整 phosphatidylinositol-3-kinase (PI3K ) 有一个中央角色的类脂化合物磷酸酶信号 transduction 串联。不过, PTEN 活动被在房间调整的机制需要进一步的说明。尽管以前的研究证明了 PTEN 的 ubiquitination 能调制它的稳定性和 subcellular 本地化,在 PTEN 功能的最批评的方面的 ubiquitination 的角色,它的磷酸酶活动,充分没被探讨。这里,我们识别 PTEN 的新奇 E3 ubiquitin ligase,沤手指蛋白质(RFP ) ,那能支持 PTEN 的不正常的 polyubiquitinations。这些 ubiquitinations 不导致 PTEN 不稳定性或本地化,但是相当显著地禁止 PTEN 磷酸酶活动因此调制它的能力调整 PI3K 信号 transduction 串联。确实, RFP overexpression 在 AKT 激活上减轻调停 PTEN 的禁止的效果;相反,调停 RNAi 内长的 RFP 击倒提高 PTEN 的能力压制 AKT 激活。而且, PTEN 的调停 RFP 的 ubiquitination 禁止小道表示的 PTEN 依赖的激活并且也压制它的能力导致 apoptosis。我们的调查结果在控制 PTEN 表明调停 RFP 的 ubiquitination 的一个关键角色活动。James T Lee Jing Shan Jiayun Zhong Muyang Li Brenda Zhou Amanda Zhou Ramon Parsons Wei Gu 2013Cell Research2013,23,4:5
20内源乙烯与1-MCP互作对番茄成熟和细胞壁物质代谢的影响显示文摘【目的】探讨内源乙烯与1-MCP的相互作用对贮藏过程中番茄成熟和细胞壁代谢的影响。【方法】将破色期番茄('佛罗里达47')果实分为4组,其中2组经低压低氧(8kPa,1.7kPaO2)处理6h后,分别立即使用50μg/L液态1-MCP(HH+1-MCP)或去离子水(HH)浸泡1min;另外2组未经HH处理的番茄果实,也分别使用50μg/L1-MCP(1-MCP)或去离子水(对照)浸泡1min,测定处理后果实在贮藏(20℃)过程中成熟相关生理指标及细胞壁组分的变化。【结果】番茄果实经HH处理后,内源乙烯含量(IEC)急剧降低至对照水平的75.6%,且对1-MCP的反应敏感性有所提高。HH+1-MCP处理显著抑制了果实硬度的下降,其硬度值在贮藏第4~16天中,平均分别较对照和1-MCP处理高29.8%和15.6%;HH+1-MCP处理果实的呼吸和乙烯峰出现时间均较对照推迟4d,较1-MCP处理推迟2d,但对峰值影响未达到显著水平;与1-MCP处理相比,HH+1-MCP处理对多聚半乳糖醛酸酶(PG)、果胶甲脂酶(PME)、α-半乳糖苷酶(α-Gal)、β-半乳糖苷酶(β-Gal)等细胞壁降解酶活性的变化影响较大,对PG的影响尤为明显;HH+1-MCP处理还显著地抑制了番茄果实贮藏期水溶性和CDTA溶性糖醛酸(UA)含量的增加,其水溶性UA含量在贮藏的第6~12天平均值分别较对照和1-MCP处理低37.3%和21.9%,其CDTA溶性UA含量在贮藏的第6~12天平均值分别较1-MCP处理果实低31.4%和20.5%;凝胶渗透色谱分析结果显示,1-MCP和HH+1-MCP处理延缓了番茄果实多聚糖醛酸分子的降解过程,且后者效果更为明显。此外,本试验HH处理各项测定指标与对照无显著差异。【结论】内源乙烯含量是调节1-MCP反应能力的重要因素,解释了不同跃变型果实在成熟起始后对1-MCP反应敏感性差异的原因。张正科 HUBER Donald J LEE James H 饶景萍 2010西北农林科技大学学报(自然科学版)2010,38,11:5
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