|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Interleukin-6 and its soluble receptor in patients with liver cirrhosis and hepatocellular carcinoma显示文摘瞄准:为了评估免疫, interleukin-6 ( IL-6 )和从有肝细胞癌( HCC )和浆液的病人的肿瘤组织标本上的 IL-6 受体( IL-6R )的组织化学的本地化与 HCC 以及肝肝硬化( LC )在一组病人 IL-6 和 sIL-6R 铺平在一组有独自一个的 LC 并且在一个控制组的病人。方法:三组题目被学习:组我(n = 83 ) 受不了 HCC 和 LC,组 II (n = 72 ) 受不了独自一个的 LC 和组 III (n = 42 ) 同样健康的控制。所有病人有丙肝病毒感染。浆液 IL-6 和 IL-6R 层次用一个商业地可得到的 ELISA 工具包被决定。Immunohistochemistry 对 IL-6 和 IL-6R 用 streptavidin-biotin 建筑群和兔子 polyclonal 抗体被执行。结果:Immunohistochemistry 分析显示出媒介到强壮细胞质并且为 IL-6 和 IL-6R 的膜反应分别地在 HCC 的至少 40% 盒子,而肝肝硬化病人和控制为 IL-6 是否定的或为 IL-6R 显示出很温和、焦点的像点的细胞质的反应。在 HCC 组的浆液 IL-6 层次比在 LC 和控制组的那些显著地高(P <
0.0001 ) 。在在 3 个组之中的 sIL-6R 集中没有有效差量。当有 HCC 的病人根据 Okuda 的分类被划分成组时, IL-6 和 sIL-6R 水平的重要浆液增加从舞台被观察我上演 III (P <
0.02, P <
0.0005 ) 。当 HCC 和 LC 病人根据孩子呸被划分成肝硬化严厉的 3 个班时,在 HCC 病人的价值比在为各相应的班的 LC 病人的那些显著地高(P <
0.01 ).CONCLUSION:在 HCC 病人的 IL-6 浆液层次比在 LC 病人和控制的那些高,建议由肿瘤的房间的这 cytokine 的增加的生产。sIL-6R 价值在所有组是类似的,仅仅在阶段 III HCC 病人增加。这些数据建议他们与肿瘤的团而非与剩余的工作有一种更靠近的关系肝的质量。 | Soresi Maurizio Giannitrapani Lydia D'Antona Fabio Florena Ada Maria La Spada Emanuele Terranova Angela Cervello Melchiorre D'Alessandro Natale Montalto Giuseppe | 2006 | World Journal of Gastroenterology2006，12，16： | 25 |
| 2 | Cyclooxygenases in hepatocellular carcinoma显示文摘许多流行病学的研究与反煽动性的药(NSAID ) 减少的 non-steroidal 表明那治疗某些恶意的发生和死亡,特别胃肠的癌症。cyclooxygenase (艇长) 酶是 NSAID 的著名目标。然而,常规 NSAID 非有选择地禁止组成的形式 COX-1,和可诱导的形式 COX-2。最近的证据显示 COX-2 是为反癌症治疗的一个重要分子的目标。它的表示在很正常的纸巾是无法发现的,并且被支持 inflammatory cytokines, mitogens,肿瘤倡导者和生长因素高度导致。COX-2 是,现在是生长得很好的长期地在上在许多恶化前表示了,恶意,并且 metastastic 癌症,包括肝细胞癌(HCC ) 。在有 HCC 的病人的 COX-2 的 Overexpression 与区分更少的 HCC 或组织学地正常的肝相比在区分得好的 HCC 通常是更高的,建议 COX-2 可以涉及 hepatocarcinogenesis 的早阶段,并且在非癌的肝织物增加了 COX-2 的表示显著地与 HCC 在病人与更短的没有疾病的幸存被联系了。在肿瘤,在层次,它影响许多机制在致癌作用包含了的前列腺素(PG ) 在 COX-2 的表示上导致增加,例如血管生成, apoptosis 的抑制,房间生长的刺激以及侵略海角和肿瘤房间的变形潜力。有选择地禁止 COX-2 (COXIB ) 的新奇代理人的可获得性,贡献了使这个分子的角色清楚些。肝癌症的动物模型上的试验性的研究证明了包括选择、非选择的 COX-2 禁止者, NSAID 象治疗学的效果一样施加 chemopreventive。然而, COX-2 禁止者由影响 HCC 细胞生长的关键机制不充分迄今为止被理解。增加的证据在 COX-2 选择禁止者的 anti-proliferative 效果建议除 COX-2 以外的分子的目标的参与。因此,艇长禁止者可以使用 COX-2-dependent 和 COX-2-independent 机制调停他们的反肿瘤性质,尽管他们向在活体内效果的相对贡献留下,更少变清。这里,我们考察艇长酶的特征,在他们可以由贡献 HCC 生长的 hepatocarcinogenesis 和机制的艇长 isoforms 的表示的角色, COX-2 选择禁止者的药理学性质,艇长禁止者的反肿瘤效果,并且为 HCC 的治疗的 COX-2 禁止者的基本原理和可行性。 | Melchiorre Cervello Giuseppe Montalto | 2006 | World Journal of Gastroenterology2006，12，32： | 24 |
| 3 | Correlation between expression of cyclooxygenase-2 and the presence of inflammatory cells in human primary hepatocellular carcinoma: Possible role in tumor promotion and angiogenesis显示文摘AIM: To investigate the association of cyclooxygenase-2(COX-2) expression with angiogenesis and the number and type of inflammatory cells (macrophages/Kupffer cells;mast cells) within primary hepatocellular carcinoma (HCC)tissues and adjacent non-tumorous (MT) tissues.METHODS: Immunohistochemistry for COX-2, CD34,CD68 and mast cell tryptase (MCT) was performed on 14 well-characterized series of liver-cirrhosis-associated HCC patients. COX-2 expression and the number of inflammatory cells in tumor lesions and surrounding liver tissues of each specimen were compared. Moreover,COX-2, CD34 staining and the number of inflammatory cells in areas with different histological degrees within each tumor sample were comparatively analyzed.RESULTS: The percentage of COX-2 positive cells was significantly higher in NT tissues than in tumors. COX-2 expression was higher in well-differentiated HCC than in poorly-differentiated tissues. Few mast cells were observed within the tumor mass, whereas a higher number was observed in the surrounding tissue, especially in peri-portal spaces of NT tissues. Abundant macrophages/Kupffer cells were observed in NT tissues, whereas the number of cells was significantly lower in the tumor mass.However, a higher cell number was observed in the well-differentiated tumor and progressively decreased in relation to the differentiation grade. Within the tumor, a positive correlation was found between COX-2 expression and the number of macrophages/Kupffer cells and mast cells. Moreover, there was a positive correlation between CD34 and COX-2 expression in tumor tissues. Comparison between well- and poorly-differentiated HCC showed that the number of CD34-positive cells decreased with dedifferentiation. However, COX-2 was the only independent variable showing a positive correlation with CD34 in a multivariate analysis.CONCLUSION: The presence of inflammatory cells and COX-2 expression in liver tumor suggests a possible relationship with tumor angiogenesis. COX-2 expressing cells and the number of macrophages/Kupffer cells and mast cells decrease with progression of the disease. | Melchiorre Cervello Daniela Foderà Ada Maria Florena Maurizio Soresi Claudio Tripodo Natale D'Alessandro Giuseppe Montalto | 2005 | World Journal of Gastroenterology2005，11，30： | 21 |
| 4 | Non invasive tools for the diagnosis of liver cirrhosis显示文摘Liver cirrhosis(LC),the end stage of many forms of chronic hepatitis of different etiologies is a diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules surrounded by annular fibrosis.This chronic progressive clinical condition,leads to liver cell failure and portal hypertension,which can favour the onset of hepatocellular carcinoma.Defining the phase of the natural history is crucial for therapeutic choice and prognosis.Liver biopsy is currently considered the best available standard of reference but it has some limits,so alternative tools have been developed to substitute liver biopsy when assessing liver fibrosis.Serum markers offer a cost-effective alternative to liver biopsy being less invasive and theoretically without complications.They can be classified into direct and indirect markers which may be used alone or in combination to produce composite scores.Diagnostic imaging includes a number of instruments and techniques to estimate liver fibrosis and cirrhosis like ultrasound(US),US Doppler,contrast enhanced US andElastography.US could be used for the diagnosis of advanced LC while is not able to evaluate progression of fibrosis,in this case Elastography is more reliable.This review aims to revise the most recent data from the literature about non invasive methods useful in defining liver fibrosis. | Maurizio Soresi Lydia Giannitrapani Melchiorre Cervello Anna Licata Giuseppe Montalto | 2014 | World Journal of Gastroenterology2014，20，48： | 15 |
| 5 | Nanotechnology applications for the therapy of liver fibrosis显示文摘Chronic liver diseases represent a major global health problem both for their high prevalence worldwide and,in the more advanced stages,for the limited available curative treatment options.In fact,when lesions of different etiologies chronically affect the liver,triggering the fibrogenesis mechanisms,damage has already occurred and the progression of fibrosis will have a major clinical impact entailing severe complications,expensive treatments and death in end-stage liver disease.Despite significant advances in the understanding of the mechanisms of liver fibrinogenesis,the drugs used in liver fibrosis treatment still have a limited therapeutic effect.Many drugs showing potent antifibrotic activities in vitro often exhibit only minor effects in vivo because insufficient concentrations accumulate around the target cell and adverse effects result as other non-target cells are affected.Hepatic stellate cells play a critical role in liver fibrogenesis,thus they are the target cells of antifibrotic therapy.The application of nanoparticles has emerged as a rapidly evolving area for the safe delivery of various therapeutic agents(including drugs and nucleic acid)in the treatment of various pathologies,including liver disease.In this review,we give an overview of the various nanotechnology approaches used in the treatment of liver fibrosis. | Lydia Giannitrapani Maurizio Soresi Maria Luisa Bondì Giuseppe Montalto Melchiorre Cervello | 2014 | World Journal of Gastroenterology2014，20，23： | 9 |
| 6 | The tumor microenvironment in hepatocellular carcinoma (Review)显示文摘 | Giulia Leonardi Saverio Candido Melchiorre Cervello Daria Nicolosi Fabio Raiti Salvatore Travali Demetrios Spandidos Massimo Libra | 2012 | International Journal of Oncology2012，，6： | 3 |
| 7 | Transcriptional regulation of miR-224 upregulated in human HCCs by NFκB inflammatory pathways显示文摘 | Cecilia Scisciani Stefania Vossio Francesca Guerrieri Valeria Schinzari Rossana De Iaco Paolo D’Onorio de Meo Melchiorre Cervello Giuseppe Montalto Teresa Pollicino Giovanni Raimondo Massimo Levrero Natalia Pediconi | 2011 | Journal of Hepatology2011，，4： | 2 |
| 8 | Identification,characterization and co-localization of label- retaining cell population in mouse endometrium with typical undifferentiated markers 显示文摘 | Cervello I Martinez-Conejero JA Horcajadas JA | 2007 | Hum Reprod2007，22，： | 1 |
| 9 | Induction of apoptosis by the proteasome inhibitor MG132 in human HCC cells: Possible correlation with specific caspase-dependent cleavage of beta-catenin and inhibition of beta-catenin-mediated transactivation 显示文摘 | Cervello M Giannitrapani L La Rosa M | 2004 | Int J Mol Med2004，13，5： | 1 |
| 10 | Resistance to di-verse apoptotic triggers in multi-drug resistant HL-60 cells andits possible relationship to the expression of P-glycoprotein,Fasand of the novel anti-apoptosis factors IAP显示文摘 | Notarbartolo M Cervello M Dusonehet L | 2003 | Cancer Lett2003，180，： | 1 |
| 11 | Resistance to diverse apoptotic triggers in multidrug resistant HL60 ceils and its possible relationship to the expression of P-glycoprotein, Fas and of the novel antiapoptosis factors IAP ( inhibitory of apoptosis proteins ) 显示文摘 | Notarbartolo M Cervello M Dusonchet L | 2002 | Cancer Lett2002，180，1： | 1 |
| 12 | Identification, characterization and co-localization of label- retaining cell population in mouse endometrium with typical undifferentiated markers显示文摘 | Cervello I Martinez-Conejero J A Horcajadas J A | 2007 | Hum Reprod2007，22，1： | 1 |
| 13 | Serum concentration of E-selectin in patients with chronic hepatitis,liver cirrhosis and hepatocellular carcinoma显示文摘 | Cervello M Virruso L Lipani G | 2000 | Cancer Res Clin Oncol2000，126，： | 1 |
| 14 | The tumor mieroenvironment in hepatocellular carcinoma (review) 显示文摘 | Leonardi GC Candido S Cervello M | 2012 | Int J 0ncol2012，40，6： | 1 |
| 15 | Resistance to diverse apoptotic triggers in multidrug resistant HL-60 cells and its possible factors IAP (inhibitory of apoptosis proteins)显示文摘 | Natarbartolo M Cervello M Dusonchet L | 2002 | Cancer Lett2002，180，： | 1 |
| 16 | Induction of apoptosis by the proteasome inhibitor MG132 in human HCC cells: Possible correlation specific carcase - dependent cleavage of beta - catenin and inhibition of beta - catenin - mediated transactivation显示文摘 | Cervello M annitrapani L Rosa M | 2004 | Int J Mol Med2004，3，5： | 1 |
| 17 | Epidemiology, risk factors, and natural history of hepatocellular carcinoma显示文摘 | MONTALTO G CERVELLO M GIANNITRAPANI L | 2002 | Ann N Y Acad Sci2002，963，： | 1 |
| 18 | Epidemiology, risk factors, and natural history of hepatocellular carcinoma 显示文摘 | Montaho G Cervello M Giannitrapani L | 2002 | Ann N Y Acad Sci2002，963，： | 1 |
| 19 | Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy显示文摘 | James A. McCubrey Linda S. Steelman Stephen L. Abrams Negin Misaghian William H. Chappell Jorg Basecke Ferdinando Nicoletti Massimo Libra Giovanni Ligresti Francac Stivala Danijela Maksimovic-Ivanic Sanja Mijatovic Giuseppeo Montalto Melchiorre Cervello P | 2012 | Current Pharmaceutical Design2012，，13： | 1 |
| 20 | Circulating intercellular adhesion molecule-1 in patients with hepatocellular carcinoma C显示文摘 | Soresi M Cervello M Lipani G | 1997 | Eur J Gastroenterol Hepatol1997，9，8： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员