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Li B.,Liver Fibrosis Diagnosis and Treatment Center | Ji Y.J.,Liver Disease Center for Military Staff | Shao Q.,Liver Fibrosis Diagnosis and Treatment Center | Zhu Z.,Hepatobiliary Surgery Center | And 3 more authors.
Experimental and Therapeutic Medicine | Year: 2015

The aim of the present study was to evaluate and compare the treatment efficacy and cost of two therapies, splenectomy and thrombopoietin, in order to optimize the treatment plans for patients with HCV-associated cirrhosis. A prospective randomized controlled trial was conducted on 69 patients with a platelet count <60,000/mm3 that were enrolled between 2009 and 2013, including 38 cases as the research group and 31 cases as the observed group. The study included two stages: A 4-week initial treatment and a 48-week antiviral treatment, during which a number of parameters were evaluated, including platelet count, liver stiffness measure, albumin, total bilirubin, alanine aminotranferase and treatment cost-effectiveness. Of the 38 patients, 21 underwent a splenectomy and their platelet counts increased to 60,000/mm3 after the 4-week initial treatment. The patients then started a 48-week P-R antiviral treatment, and 18 cases completed the treatment. In addition, 17/38 patients received thrombopoietin as a drug therapy. The platelet counts in 15 cases increased to >60,000/mm3 and the patients received antiviral treatment, among which 9 cases completed the second treatment stage. The expense of the splenectomy group treatment was higher compared with that received by the thrombopoietin group. The results of the present study indicated that splenectomy was more effective at increasing platelet count. More splenectomy patients completed the full course of antiviral treatment and presented a sustained virologic response, compared with the thrombopoietin group. Therefore, splenectomy may be more expensive compared with thrombopoietin; however, the improved efficacy suggests that on balance it is the preferable treatment option. © 2015, Spandidos Publications. All rights reserved. Source


Li Z.,Shanghai University | Wang J.,Zhejiang Police College | Zhou T.,Hepatobiliary Surgery Center | Ye X.,Ningbo Institute of Medical science
Oncology Letters | Year: 2016

The aim of the present study was to establish a model of tumor cell growth and visualize HIF-1α overexpression in a nude mouse xenograft model of colorectal cancer (CRC). In the study, HIF-1α lentiviral vector and helper plasmid were co-transfected into 293T packaging cells using a liposome method, and the virus was collected following transfection and used to infect CRC SW480, SW620, LoVo and HCT116 cells. Puromycin was used for the selection and large-scale amplification of the stable HIF-1α expression of green fluorescent protein (GFP)-positive cells. HIF-1α-expressing cells were injected intraperitoneally into a nude mouse xenograft model, and resulting tumor nodules was separated and confirmed using an inverted fluorescence microscope. The results demonstrated that HIF-1α was not expressed in CRC cells in normoxic conditions. When treated with CoCl2, the expression of HIF-1α could be induced in all the cancer cell lines, except SW480. HIF-1α was highly expressed following infection with lentiviral particles. Stable expression of HIF-1α promoted migration in the SW480 cells. Following intraperitoneal injection of nude mice with SW480-HIF-1α, a significant number of tumor nodules formed in the intestinal wall compared with the controls (P<0.05). The successful construction of the dual expression HIF-1α and GFP visualization xenograft model provides a good foundation for the screening of HIF-1α-related functions and for investigating the therapeutic potential of drugs that target HIF-1α. © 2016, Spandidos Publications. All rights reserved. Source


Zhang C.,Soochow University of China | Yang G.,Shanghai University | Lu D.,Ningbo University | Ling Y.,Soochow University of China | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2014

The aim of the present study was to investigate the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in acute rejection reaction (ARR) following orthotopic liver transplantation in a rat model. Serum VEGF and bFGF levels were detected using ELISA, and their expression levels in liver and spleen tissues were determined using immunohistochemistry. The mRNA expression levels of VEGF and bFGF were detected by conducting a quantitative polymerase chain reaction during the ARR following orthotopic liver transplantation. The expression levels of VEGF and bFGF in the serum 3 days following liver transplantation were significantly higher compared with those in the other groups (1 and 7 days following transplantation; P<0.01). In addition, the numbers of cells in the liver tissue that were shown to be positive for the expression VEGF and bFGF using immunohistochemistry were significantly higher 3 days following transplantation than at the other time points (P<0.0001). Furthermore, the numbers of cells positive for VEGF and bFGF expression in the spleen detected 3 days following the transplantation surgery were also significantly higher compared with those at the other time points (P<0.01). VEGF and bFGF mRNA expression levels were also increased from 1 day following the surgery and reached a peak at day 3, prior to declining gradually and remaining at a relatively high level. VEGF and bFGF mRNA expression levels changed dynamically, by peaking and then declining, in ARR following orthotopic liver transplantation. These changes may have an important impact on angiogenesis and the inflammatory reaction, and the identification of these changes increases the current understanding of ARR following orthotopic liver transplantation. Source


Cai W.-K.,Kunming General Hospital | Zhang J.-B.,Hepatobiliary Surgery Center | Wang N.-M.,Xian Jiaotong University | Wang Y.-L.,Central South University | And 3 more authors.
Scientific World Journal | Year: 2015

Histamine Hreceptor (HRH2) was previously suggested to affect the proliferation of breast cancer cells and disease-free survival of breast cancer patients. Furthermore, a common polymorphism, rs2067474, was identified in an enhancer element of the HRH2 gene promoter and was reported to be associated with various diseases including cancer. However, the relationship between this polymorphism and breast cancer risk and malignant degree remains unclear. The aim of this study was to clarify the clinical association of rs2067474 polymorphism with breast cancer. A total of 201 unrelated Chinese Han breast cancer patients and 238 ethnicity-matched health controls were recruited and rs2067474 polymorphism was genotyped. Logistic regression analyses were performed to calculate the odds ratios (ORs) as a measure of association of genotype with breast cancer according to 3 genetic models (dominant, recessive, and additive). Although the percentage of hormone receptor negative cases tended to be higher in AA genotypes, we did not find any significant associations of rs2067474 polymorphism with breast cancer risk or with related clinicopathological parameters in the present study, which indicates that rs2067474 polymorphism of HRH2 gene might not be a risk factor in the development of breast cancer in Chinese Han population. Copyright © 2015 Wen-Ke Cai et al. Source


Yang L.,Hepatobiliary Surgery Center | Ma Z.,TaiAn Center Hospital | Wang D.,Hepatobiliary Surgery Center | Zhao W.,Hepatobiliary Surgery Center | And 2 more authors.
Cancer Biology and Therapy | Year: 2010

Aims: It is important to understand the role of microRNA in the transformation from chronic HBV hepatitis to hepatocellular carcinoma in hepatocarcinogenesis. Relationship of microRNA-602 with chronic HBV hepatitis, liver cirrhosis and HCC was investigated in this article. Results: (1) 14 MicroRNAs were aberrantly expressed in HCC and CL compared with NL. Among these, microRNA-602 expression in CH, LC, NT and HCC was 2.939, 3.234, 2.439 and 4.134 times of that in NL respectively, which was significantly different (p < 0.01 for all vs. NL); RASS F1A expression in LC and HCC was lower than that in NL, while P73 protein expression in CL was higher than that in NL and HCC. (2) MicroRNA-602 expression in HepG2 2.2.15 and HepG2-HBX was 2.643 and 3.48 times of that in HepG2 (p < 0.05 for both). (3) MicroRNA-602 inhibition in HepG2 cells was associated with RASS F1A mRNA and protein expression increased to 4.37, 3.01 times respectively of those not, with cell apoptosis increased and cell proliferation rate decreased significantly, changes were similar in HepG2-HBX cells. Methods: (1) MicroRNA expression was investigated in normal (NL), chronic HBV hepatitis (CH), HBV-positive cirrhotic (CL), HBV-positive HCC and corresponding normal para-tumorous livers (NT) and hepatoma cells was evaluated with microRNA microarray and verified by real-time PCR, and microRNA-602 was selected for further study. Expression of miR602-target genes RASS F1A and P73 were detected with RT-PCR and western blot. (2) MicroRNA-602 expression in HepG2 and HepG2-HBX was inhibited by miR-602 inhibitor transfection; RASS F1A and P73 expression was detected and cell apoptosis and proliferation were detected. Conclusions: MicroRNA-602 plays a procarcinogenic role in HBV-related hepatocarcinogenesis by inhibiting RASS F1A. MicroRNA-602 might be an early diagnostic marker for HBV-mediated HCC. © 2010 Landes Bioscience. Source

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