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1.
Hepatogastroenterology ; 61(133): 1192-5, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25436281

RESUMO

BACKGROUND/AIMS: To explore the surgical way of treating giant hepatic artery aneurysm(HAA). METHODOLOGY: Three hepatic artery aneurysm patients who were performed aneurysm resection without revascularization of the hepatic artery were reviewed. After surgery, the values of liver function and enhanced CT scan of the patients were followed. RESULTS: All the three patients were recovered well postoperatively and only several values of biochemistry marks of liver function as ALT, AST, TBIL and DB in one case with liver cirrhosis were elevated and decreased to normal ranges in a few days postoperatively. The values of biochemistry marks of liver function in other two cases were within normal limits. The enhanced CT scan also showed arteries in the liver after hepatic artery aneurysm resection. CONCLUSIONS: Giant HAA may be safely removed without revascularization of the hepatic artery.


Assuntos
Aneurisma Roto/cirurgia , Aneurisma/cirurgia , Artéria Hepática/cirurgia , Procedimentos Cirúrgicos Vasculares , Idoso , Aneurisma/sangue , Aneurisma/diagnóstico , Aneurisma/fisiopatologia , Aneurisma Roto/sangue , Aneurisma Roto/diagnóstico , Aneurisma Roto/fisiopatologia , Aortografia/métodos , Biomarcadores/sangue , Circulação Colateral , Hemodinâmica , Artéria Hepática/fisiopatologia , Humanos , Ligadura , Circulação Hepática , Masculino , Pessoa de Meia-Idade , Técnicas de Sutura , Tomografia Computadorizada por Raios X , Resultado do Tratamento
2.
World J Gastroenterol ; 14(44): 6802-7, 2008 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-19058305

RESUMO

AIM: To evaluate the effects of interferon-alpha-2b (IFN-alpha-2b) on expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in human hepatocellular carcinoma (HCC) inoculated in nude mice and to study the underlying mechanism of IFN-alpha-2b against HCC growth. METHODS: Thirty-two nude mice bearing human HCC were randomly divided into four groups (n = 8). On the 10th day after implantation of HCC cells, the mice in test groups (groups A, B and C) received IFN-alpha-2b at a serial dose (10000 IU for group A, 20000 IU for group B, 40000 IU for group C sc daily) for 35 d. The mice in control group received normal saline (NS). The growth conditions of transplanted tumors were observed. Both genes and proteins of COX-2 and VEGF were detected by RT-PCR and Western blot. Apoptosis of tumor cells in nude mice was detected by TUNEL assay after treatment with IFN-alpha-2b. RESULTS: Tumors were significantly smaller and had a lower weight in the IFN-alpha-2b treatment groups than those in the control group (P < 0.01), and the tumor growth inhibition rate in groups A, B and C was 27.78%, 65.22% and 49.64%, respectively. The expression levels of both genes and proteins of COX-2 and VEGF were much lower in the IFN-alpha-2b treatment groups than in the control group (P < 0.01). The apoptosis index (AI) of tumor cells in the IFN-alpha-2b treatment groups was markedly higher than that in the control group (P < 0.01). Group B had a higher inhibition rate of tumor growth, a lower expression level of COX-2 and VEGF and a higher AI than groups A and C (P < 0.05), but there was no significant difference between groups A and C. CONCLUSION: The inhibitory effects of IFN-alpha-2b on implanted tumor growth and apoptosis may be associated with the down-regulation of COX-2 and VEGF expression. There is a dose-effect relationship. The medium dose of IFN-alpha-2b for inhibiting tumor growth is 20000 IU/d.


Assuntos
Antineoplásicos/farmacologia , Carcinoma Hepatocelular/tratamento farmacológico , Ciclo-Oxigenase 2/metabolismo , Interferon-alfa/farmacologia , Neoplasias Hepáticas/tratamento farmacológico , Fator A de Crescimento do Endotélio Vascular/metabolismo , Animais , Apoptose/efeitos dos fármacos , Carcinoma Hepatocelular/enzimologia , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Ciclo-Oxigenase 2/genética , Relação Dose-Resposta a Droga , Regulação para Baixo , Feminino , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Interferon alfa-2 , Neoplasias Hepáticas/enzimologia , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , RNA Mensageiro/metabolismo , Proteínas Recombinantes , Fator A de Crescimento do Endotélio Vascular/genética
3.
Cancer Biomark ; 15(4): 507-13, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25792469

RESUMO

BACKGROUND: MicroRNA-145 (miR-145) plays a crucial role in cancer prognosis. OBJECTIVE: This study aimed to investigate the prognostic value of miR-145 in patients with various cancers. METHODS: We pooled published literature from PubMed, EMBASE, Web of Science and Cochrane Database of Systematic Reviews and calculated the hazard ratios (HRs) with 95% confidence intervals (CIs) to estimate the correlation between miR-145 expression levels and survival of patients with general cancers. RESULTS: A total of 615 cases from 8 studies of multiple cancers were examined in this meta-analysis. The HR for overall survival (OS) of low miR-145 expression in multiple cancers was 1.80 (95% CI = 1.19-2.70). Furthermore, after excluding 1 study for its potential heterogeneity, the results suggested an increasing prognostic value of low miR-145 expression (HR = 2.20, 95% CI = 1.63-1.97). In addition, there was no significant difference between miR-145 expression levels and recurrence-free survival (RFS). CONCLUSION: In conclusion, our findings suggest that miR-145 expression is associated with OS in cancer patients and can serve as a promising biomarker for monitoring prognosis.


Assuntos
Biomarcadores Tumorais/biossíntese , MicroRNAs/biossíntese , Neoplasias/genética , Prognóstico , Biomarcadores Tumorais/genética , Intervalo Livre de Doença , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , Neoplasias/patologia
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