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88篇 您的检索式:作者名="Sferra"
    题名 作者 年代 出处 被引量
1清化肠饮对溃疡性结肠炎小鼠TLR4/NF-κB通路的影响显示文摘[目的]评价清化肠饮对溃疡性结肠炎(UC)的治疗效果并阐明其可能的分子机制。[方法]利用葡聚糖硫酸钠(DSS)诱导UC小鼠模型,将动物随机分为3组:正常对照组、UC模型组和清化肠饮治疗组,每组各10只。观察小鼠疾病活动指数、组织病理学改变,测量血清淀粉酶样蛋白A(SAA)水平,以及观察清化肠饮对UC小鼠模型中TLR4、MyD88、IκB磷酸化表达水平,NF-κB核转录的影响。[结果]研究发现清化肠饮能够很好地改善DSS诱导UC小鼠模型的临床症状、结肠缩短和组织损伤。此外,经清化肠饮的治疗能明显降低DSS诱导的SAA的分泌。此外,清化肠饮能明显抑制DSS诱导的TLR4的表达和MyD88、IκB的磷酸化和NF-κB的核易位。[结论]抑制TLR4/NF-κB通路可能是清化肠饮治疗UC的机制之一。方文怡 柯晓 周凡 高尤亮 谢冰颖 胡光宏 彭军 陈友琴 THOMAS J SFERRA 2014中国中西医结合消化杂志2014,22,8:7
2清达颗粒对AngⅡ诱导的高血压小鼠肾脏损害的干预研究显示文摘目的:探讨清达颗粒对AngⅡ诱导的高血压肾损伤小鼠血压及相关病理的影响。方法:将18只小鼠随机分为3组:对照组、模型组及给药组,其中模型组及给药组予AngⅡ通过植入式胶囊渗透压泵连续灌注28d以建立高血压模型。给药组予清达颗粒灌胃给药,剂量为22. 9mg/天/0. 2ml,对照组和模型组予等体积的生理盐水灌胃,每天1次,连续给药28d。结果:与模型组对比,清达颗粒能够抑制血压的升高幅度,差异具有统计学意义(P <0. 05);与模型组比较,清达颗粒能够明显改善肾小动脉及肾小球硬化,降低肾小球内胶原阳性比例(P <0. 05)。结论:清达颗粒能降低AngⅡ诱导的高血压小鼠的血压、减轻肾脏损伤。杨美玲 周雪玲 彭美中 卢妍 彭军 陈友琴 Thomas Joseph SFERRA 褚剑锋 2019中医药通报2019,18,2:5
3Smad3 knock-out mice as a useful model to study intestinal fibrogenesis显示文摘瞄准:为了在形态学和免疫评估可能的差别, CD3,转变生长因素 beta1 (TGF-beta1 ) , Smad7, alpha 光滑的肌肉肌动朊(alpha-Sma ) ,和骨胶原的组织化学的表示打 I-VII 小并且在 Smad3 空、野类型的老鼠的大肠。方法:十 0 和十只野类型的成年老鼠在年龄和机关的 4 瞬间被牺牲(食管,小、大的肠,输尿管) 为组织学被收集(苏木精和曙红,马森 thrichrome,染色的银) ,形态测定法和免疫组织化学分析。肠的织物 homogenates 的 TGF-beta1 层次被 ELISA 估计。结果:没有宏观的肠的损害在空、野类型的老鼠两个都被检测。组织学并且 morphometric 评估在肌肉层厚度揭示了重要减小小并且在空老鼠的大肠同样与野类型的老鼠相比。Immunohistochemistry 评估显示出染色在的 CD3+ T 房间, TGF-beta1 和 Smad7 的重要增加小并且 Smad3 空老鼠的大肠粘膜同样与野类型的老鼠相比。染色的 Alpha-Sma 和骨胶原 I-VII 小并且大肠没在二组老鼠之间不同。结肠的织物 homogenates 的 TGF-beta1 层次比在野类型的老鼠在空老鼠是显著地更高的。在初步的实验,导致 TNBS 的肠的纤维变性的重要减小作为与野类型的老鼠相比在空老鼠被观察。结论:Smad3 空老鼠是一个有用模型调查在肠的发炎和纤维变性表明小径的 TGF-beta/Smad 的在活体内角色。Giuliana Zanninelli Antonella Vetuschi Roberta Sferra Angela D'Angelo Amato Fratticci Maria Adelaide Continenza Maria Chiaramonte Eugenio Gaudio Renzo Caprilli Giovanni Latella 2006World Journal of Gastroenterology2006,12,8:3
4Acid‐suppressive therapy is associated with spontaneous bacterial peritonitis in cirrhotic patients: A meta‐analysis显示文摘Abhishek Deshpande Vinay Pasupuleti Priyaleela Thota Chaitanya Pant Sulaiman Mapara Sohaib Hassan David D K Rolston Thomas J Sferra Adrian V Hernandez 2013J Gastroenterol Hepatol2013,,2:3
5熊果酸通过靶向STAT3信号通路对葡聚糖硫酸钠诱导的小鼠溃疡性结肠炎的保护作用显示文摘目的:研究熊果酸(UA)对葡聚糖硫酸钠(DSS)诱导的实验性小鼠结肠炎模型的抗炎作用,旨在阐明其对肠上皮细胞(IEC)作用的可能分子机制。方法:在体内研究中,将体质量为20~22 g的雄性BALB/c小鼠15只采用随机数字表法分为正常对照组、DSS模型组、DSS+熊果酸治疗组。通过3%DSS诱导8 d,制备小鼠结肠炎模型;其中一组DSS诱导的小鼠结肠炎模型采用UA预处理。各实验组的小鼠体质量和结肠长度分别采用物理天平和游标卡尺测定;参照临床疾病活动指数(DAI)评分法对小鼠进行评分。采用HE染色观察各组结肠组织病理学变化;通过ELISA法测定各组小鼠血液中血清淀粉样蛋白酶A和结肠组织中IL-6的水平。以IL-6刺激分化的Caco-2细胞制备体外人肠上皮细胞炎症模型,通过Western blot检测UA对肠上皮细胞IL-6/STAT3信号通路中STAT3磷酸化的影响。结果:①与正常对照组比较,DSS模型组的DAI评分增加、结肠长度缩短和组织损伤明显,差异均具有统计学意义(P<0.05);与DSS模型组比较,UA显著抑制了DSS诱导的DAI评分增加、结肠长度缩短和组织学损伤,差异均具有统计学意义(P<0.05)。②与正常对照组比较,DSS模型组的血清淀粉酶(SAA)水平和结肠组织中IL-6水平升高明显,差异均具有统计学意义(P<0.05);与DSS模型组比较,UA可显著逆转DSS诱导的血清淀粉酶(SAA)水平和结肠IL-6水平的升高,差异均具有统计学意义(P<0.05)。③与正常肠上皮细胞比较,IL-6刺激显著上调STAT3的磷酸化水平;而UA可显著抑制肠上皮细胞中IL-6诱导的STAT3磷酸化水平的增加,差异具有统计学意义(P<0.05)。结论:熊果酸可通过阻断IL-6/STAT3信号通路改善了DSS诱导的结肠炎,提示熊果酸在靶向治疗溃疡性结肠炎中可能具有临床应用潜力。庄群川 沈阿灵 刘丽雅 SANKARARAMAN Senthilkumar SFERRA Thomas Joseph 陈骐 陈友琴 2021康复学报2021,31,1:1
6Delayed tension pneumothorax complicating central venous catheterization and positive pressure ventilation显示文摘Plewa MC Ledrick D Sferra JJ 1995Am J Emerg Med1995,13,5:1
7Smad3-null mice lack interstitial cells of Cajal in the colonic wall显示文摘Vetuschi A Sferra R Latella G 2006Eur J Clin Invest2006,36,1:1
8Complications of missed or untreated Lisfrane injuries 显示文摘Philbin T Rosenberg'G Sferra JJ 2003Foot Ankle Clin2003,8,1:1
9Adano-associaled virus-mediated gene transfer to the brain: duration and modulation of expression显示文摘LO WD QU G SFERRA TJ 1999Hum Gene Ther1999,10,:1
10Targeted disruption of Smad3 confers resistance to the development of dimethvlnitrosamine-induced hepatic fibrosis in mice显示文摘Latella G Vetuschi A Sferra R 2009Liver Intemational2009,29,7:1
11The efficacy of oral nons- teroidal anti-inflammatory medication(NSAID) in the treatmentof plantar fasciitis ;a randomized,prospective,placebocontrolled study显示文摘l)onley B G Moore T Sferra J 2007Foot Ankle lnt2007,28,:1
12Microsphere-adenoviral complexes target and transduce the glomerulus in vivo显示文摘Nahman NS Sferra TJ Kronenberger J 2000Kidney Int2000,58,4:1
13Complications of missed or untreated Lisfranc injuries显示文摘Philbin T Rosenberg G Sferra J J 2003Foot Ankle Clin2003,8,1:1
14Glomerular beta-galactosidase expression following transduction with microsphere-adenoviral complexes显示文摘Bhatt UY Sferra TJ Johnson A 2002Kidney Int2002,611,:1
15Neuropilin-VEGF sig- naling pathway acts as a key modulator of vascular, lymphatic, and inflammatory cell responses of the bladder to intravesical BCG treatment 显示文摘Saban M R Sferra T J Davis C A 2010Am J Physiol Renal Physiol2010,299,6:1
16Pien Tze Huang(片仔癀) Overcomes Doxorubicin Resistance and Inhibits Epithelial-Mesenchymal Transition in MCF-7/ADR Cells显示文摘Objective: To evaluate the effect of Pien Tze Huang (片仔癀, PZH) on breast cancer chemo resistance and related epithelial-mesenchymal transition (EMT) and investigate the underlying mechanisms. Methods: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to determine the cell viability. Adriamycin (ADR) staining observed by fluorescence microscope was performed to detect the accumulation of ADR. Transwell assay was used to analyze the cell migration and invasion. Western-blot was performed to detect the protein expression of related genes. Results: MCF-7/ADR cells were resistant to ADR treatment, and PZH treatment inhibited the viability of MCF-7/ADR cells in a dose-dependent manner. PZH treatment also increased the intercellular accumulation of ADR and down-regulated the expression of ABCG2 and ABCB1 in MCF-7/ADR cells (P<0.05). In addition, PZH treatment inhibited EMT, migration and invasion of MCF-7/ADR cells (P<0.05). Moreover, PZH suppressed activation of transforming growth factor β 1 (TGF-β) signaling in MCF-7/ADR cells (P<0.05). Conclusion: PZH treatment can effectively overcome chemoresistance via down-regulating ABCG2, ABCB1 and inhibit EMT in ADR resistant human breast cancer cells via suppression of the TGF-β 1 pathway.CHEN Xi QI Fei SHEN A-ling CHU Jian-feng Thomas Joseph Sferra CHEN You-qin PENG Jun 2019Chinese Journal of Integrative Medicine2019,25,8:1
17Prevention of colonic fibrosis by Boswellia and Scutellaria extracts in rats with colitis induced by 2,4,5-trinitrobenz -ene sulphonic acid显示文摘Latella G Sferra R Vetuschi A 2008Eur J Clin Invest2008,38,6:1
18Complications of missed or untreated Lisfranc injuries显示文摘Philbin T Rosenberg G Sferra J J 2003Foot Ankle Clin2003,8,1:1
19Prevention of colonic fibrosis by Boswellia and Seutellaria extracts in rats with colitis induced by 2, 4, 5-trinitrobenzene sulphonic acid 显示文摘Latella G Sferra R Vetusehi A 2008Eur J Clin Invest2008,38,6:1
20Smad3 loss con- fers resistance to the development of trinitrobenzene sulfon- ic acid-induced colorectal fibrosis 显示文摘Latella G Vetuschi A Sferra R 2009Eur J Clin Invest2009,39,:1
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