|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Mi R-122 in hepatitis B virus and hepatitis C virus dual infection显示文摘Hepatitis B virus(HBV) and hepatitis C virus(HCV) infections are the most common causes of chronic liver diseases and hepatocelluar carcinomas. Over the past few years, the liver-enriched micro RNA-122(mi R-122) has been shown to differentially regulate viral replication of HBV and HCV. It is notable that thelevel of mi R-122 is positively and negatively regulated by HCV and HBV, respectively. Consistent with the welldocumented phenomenon that mi R-122 promotes HCV accumulation, inhibition of mi R-122 has been shown as an effective therapy for the treatment of HCV infection in both chimpanzees and humans. On the other hand, mi R-122 is also known to block HBV replication, and HBV has recently been shown to inhibit mi R-122 expression; such a reciprocal inhibition between mi R-122 and HBV suggests an intriguing possibility that mi R-122 replacement may represent a potential therapy for treatment of HBV infection. As HBV and HCV have shared transmission routes, dual infection is not an uncommon scenario, which is associated with more advanced liver disease than either HBV or HCV mono-infection. Thus, there is a clear need to further understand the interaction between HBV and HCV and to delineate the role of mi R-122 in HBV/HCV dual infection in order to devise effective therapy. This review summarizes the current understanding of HBV/HCV dual infection, focusing on the pathobiological role and therapeutic potential of mi R-122. | Kyoungsub Song Chang Han Srikanta Dash Luis A Balart Tong Wu | 2015 | World Journal of Hepatology2015，7，3： | 6 |
| 2 | 以肝脏为靶器官的基因治疗时重组腺病毒引起的急性肝炎显示文摘目的 研究腺病毒为载体的基因治疗时淋巴细胞在肝组织免疫反应中的作用,探讨免疫抑制疗法在腺病毒载体基因治疗中的可行性。 方法 取8只恒河猴,经不同路径输入携带大肠杆菌lacZ基因或荧火虫荧光素酶基因luc的重组腺病毒6只。其中4只进行免疫抑制治疗。将含lacZ的质粒DNA注入2只动物作为对照。用免疫组织化学法检测β2-MG、HLA-DR、CD3、CD4、CD8及CD20。 结果 腺病毒介导的基因治疗时肝脏的β2-MG、HLA-DR、CD3、CD4及CD8阳性细胞明显增多。腺病毒载体和转基因均与肝损害有关, 表现为一过性, 呈轻、中度无黄疸性肝炎。免疫抑制的动物只要处于免疫抑制状态下就没有肝炎的表现,基因表达的时间延长。质粒介导的基因转导效果差, 无肝损害及免疫反应。所有动物B淋巴细胞抗原CD20始终阴性。 结论 腺病毒介导的基因治疗时肝脏的β2-MG、HLA-DR、CD3、CD4及CD8阳性细胞明显增多, 造成轻、中度一过性肝损害。使用免疫抑制药物可避免肝损害的发生并延长基因表达的时间。 | 鲁慧英 Deborah Sullivan Srikanta Dash Michael A Gerber | 2001 | 中华肝脏病杂志2001，9，5： | 3 |
| 3 | Hepatocellular carcinoma xenograft supports HCV replication:A mouse model for evaluating antivirals显示文摘AIM: To develop a hepatocellular carcinoma (HCC) xenograft model for studying hepatitis C virus (HCV) replication in a mice, and antiviral treatment.METHODS: We developed a stable S3-green fluorescence protein (GFP) cell line that replicated the GFP-tagged HCV sub-genomic RNA derived from a highly efficient JFH1 virus. S3-GFP replicon cell line was injected subcutaneously into γ-irradiated SCID mice. We showed that the S3-GFP replicon cell line formed human HCC xenografts in SCID mice. Cells were isolated from subcutaneous tumors and then serially passaged multiple times in SCID mice by culturing in growth medium supplemented with G-418. The mouse-adapted S3-GFP replicon cells were implanted subcutaneously and also into the liver of SCID mice via intrasplenic infusion to study the replication of HCV in the HCC xenografts. The tumor model was validated for antiviral testing after intraperitoneal injection of interferon-α (IFN-α). RESULTS: A highly tumorigenic S3-GFP replicon cell line was developed that formed subcutaneous tumors within 2 wk and diffuse liver metastasis within 4 wk in SCID mice. Replication of HCV in the subcutaneous and liver tumors was confirmed by cell colony assay, detection of the viral RNA by ribonuclease protection assay and real-time quantitative reverse transcription polymerase chain reaction. High-level replication of HCV sub-genomic RNA in the tumor could be visualized by GFP expression using fluorescence microscopy. IFN-α cleared HCV RNA replication in the subcutaneous tumors within 2 wk and 4 wk in the liver tumor model. CONCLUSION: A non-infectious mouse model allows us to study replication of HCV in subcutaneous and metastatic liver tumors. Clearance of HCV by IFN-α supports use of this model to test other anti-HCV drugs. | Sidhartha Hazari Henry J Hefler Partha K Chandra Bret Poat Feyza Gunduz Tara Ooms Tong Wu Luis A Balart Srikanta Dash | 2011 | World Journal of Gastroenterology2011，17，3： | 2 |
| 4 | Increased Expression of P-Glycoprotein and Doxorubicin Chemoresistance of Metastatic Breast Cancer Is Regulated by miR-298显示文摘 | Lili Bao Sidhartha Hazari Smriti Mehra Deepak Kaushal Krzysztof Moroz Srikanta Dash | 2012 | The American Journal of Pathology2012，，6： | 1 |
| 5 | 以肝脏为靶器官的基因治疗时腺病毒引起的急性肝炎(英文)显示文摘目的 确定以肝脏为靶器官的基因治疗时急性肝炎的机制。方法 用HE法和免疫组织化学法对 8只恒河猴通过不同径路接受以腺病毒或Lipofectamine为载体的基因治疗时的免疫反应进行了研究。结果 经静脉或胆管注入除去E1,携带lacZ基因的腺病毒后 1至 3周发生了轻到中度急性肝炎。有病变的肝脏内CD3+,CD4 +和CD8+T细胞明显增多而B细胞缺如。肝细胞表面 β2 MG和HLA DR也增多。免疫抑制治疗使急性肝炎和伴随的免疫反应延迟。结论 腺病毒介导的基因治疗时肝脏的免疫反应是T细胞介导的 ,主要受I型MHC限制。腺病毒载体和转基因均与肝损害有关。肝脏损害呈轻、中度 ,是可逆的。免疫抑制药物可延迟免疫性肝损害的发生并延长基因表达的时间。 | 鲁慧英 Deborah Sullivan Michael A Gerbera Srikanta Dash | 2002 | Chinese Medical Journal2002，，5： | 1 |
| 6 | Interferon alpha induced intrahepatic pSTAT1 inversely correlate with serum HCV RNA levels in chronic HCV infection显示文摘 | Feyza Gunduz Chaithanya Mallikarjun Luis A. Balart Srikanta Dash | 2014 | Experimental and Molecular Pathology2014，，1： | 1 |
| 7 | Increased Expression of P-Glycoprotein and Doxorubicin Chemoresistance of Metastatic Breast Cancer Is Regulated by miR-298显示文摘 | Lili Bao Sidhartha Hazari Smriti Mehra Deepak Kaushal Krzysztof Moroz Srikanta Dash | 2012 | The American Journal of Pathology2012，，6： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员