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1.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao ; 36(4): 394-9, 2014 Aug.
Artigo em Zh | MEDLINE | ID: mdl-25176208

RESUMO

OBJECTIVE: To observe the hemodynamic change and reperfusion injury cause by transient hepatic venous occlusion and transient hepatic inflow occlusion in rats. METHODS: The rat liver was divided into 3 different areas: the ischemia reperfusion (IR) area: the inflow of the right superior lobe was clamped for half an hour; the non-isolated lobe congestive reperfusion (NIL-CR) area: the outflow of the right median lobe was clamped for half an hour; and the isolated lobe congestive reperfusion (IL-CR) area: the outflow of the left lobe was clamped for half an hour. The flux value and the oxygen saturation of microcirculation were monitored before at clamping for 30 minutes, and on 1 day, 3 days ,and 7 days after reperfusion. The hepatic damage and Suzuki's score were evaluated. RESULTS: After clamping for 30 minutes, the flux value in the IR area was significantly higher than in NIL-CR area (P<0.01) and IL-CR area (P<0.01), the oxygen saturation in the IR area was significantly higher than in NIL-CR area (P<0.01) and IL-CR area (P<0.05). Compared with IR area, both NIL-CR area and IL-CR area were found having more severe liver damage in terms of Suzuki's score in early postoperative period (at clamping for 30 minutes and on 1 day, P<0.01). However, there was no significant difference between NIL-CR area and IL-CR area in flux value, oxygen saturation, and Suzuki's score (P>0.05). CONCLUSIONS: Hepatic venous occlusion can more effectively decrease the blood perfrusion and oxygen saturation; thus, compared to the IR, CR can result in more severe liver damage. The presence of normal liver tissue around the congestion area can not influence liver damage in transient hepatic venous occlusion.


Assuntos
Fígado/fisiopatologia , Traumatismo por Reperfusão/fisiopatologia , Animais , Modelos Animais de Doenças , Hemodinâmica , Veias Hepáticas , Masculino , Microcirculação , Ratos , Ratos Sprague-Dawley
2.
ANZ J Surg ; 86(10): 816-820, 2016 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25088384

RESUMO

BACKGROUND: Transarterial chemoembolization (TACE) is commonly used to treat advanced hepatocellular carcinoma (HCC), but less is known regarding safety and efficacy of TACE in patients with HCC and portal vein tumour thrombosis (PVTT). The objective of this study was to evaluate the effect of TACE treatment on 1-year survival in patients with HCC and PVTT. METHODS: Medline, EMBASE, CENTRAL databases (until July 2013) were searched for studies that evaluated the efficacy of TACE with regard to survival in patients with HCC and PVTT. One-year survival rate, the primary end point, was compared between patients who received TACE and those who received control treatment. RESULTS: Five prospective studies were identified that assessed the efficacy of TACE on survival. These studies included 600 patients: 335 received TACE therapy and 226 received control treatments. Three of the five studies reported 1-year survival data and were used in the meta-analysis. The combined odds ratio (3.079, 95% confidence interval = 1.094-8.662) indicated that patients who received TACE had a significantly better 1-year survival rate compared with patients in the control group (P = 0.033). CONCLUSIONS: There are several limitations to this analysis that should be considered when interpreting the findings. The studies used different treatment regimens as controls or with TACE. These differences across the studies may have altered the 1-year survival outcomes in each study and confounded our analysis. This meta-analysis showed that TACE improves the 1-year survival of patients with HCC and PVTT. However, additional prospective controlled trials are required to further substantiate these findings.


Assuntos
Carcinoma Hepatocelular/terapia , Quimioembolização Terapêutica , Neoplasias Hepáticas/terapia , Veia Porta , Trombose Venosa/etiologia , Antineoplásicos/administração & dosagem , Carcinoma Hepatocelular/complicações , Carcinoma Hepatocelular/mortalidade , Humanos , Neoplasias Hepáticas/complicações , Neoplasias Hepáticas/mortalidade , Análise de Sobrevida , Resultado do Tratamento
3.
Oncol Rep ; 33(3): 1493-8, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25571964

RESUMO

Despite advances in the detection and treatment of hepatocellular carcinoma (HCC), the prognosis remains poor partly due to recurrence or extra/intrahepatic metastasis. Stem­like cancer cells are considered the source of malignant phenotypes including metastasis in various types of cancer. HCC side population (SP), considered as stem­like cancer cells, plays an important role in the migration and invasion in HCC, while the mechanisms involved remain unknown. In the present study, high levels of STAT3 and phospho­STAT3 were observed in MHCC97H SP cells compared with the main population (MP) cells. Inhibition of phospho­STAT3 led to a reduction of miR­21 expression, an increase of PTEN, RECK, and programmed cell death 4 (PDCD4) expression as well as the migration and invasion of SP cells. A set of rescue experiments was performed using different combinations of STAT3 inhibitor, miR­21 mimics and siRNAs to observe the expression of miR­21 targets, cell migration and invasion alterations. Data indicated that the alterations induced by STAT3 inhibition were partly reversed by the upregulation of miR­21. Additionally, the cells migration and invasion when silencing the targets of miR­21 were also reversed by STAT3 inhibition. In conclusion, the present study revealed the aberrant expression of STAT3 and miR­21 in HCC SP cells. Targeting STAT3 may limit HCC migration and invasion, which is likely to involve the regulation of miR­21 and its targets PTEN, RECK and PDCD4. Strategies directed towards STAT3 may therefore be a novel approach for the treatment of HCC.


Assuntos
Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia , MicroRNAs/biossíntese , Células-Tronco Neoplásicas/patologia , Fator de Transcrição STAT3/antagonistas & inibidores , Apoptose/efeitos dos fármacos , Proteínas Reguladoras de Apoptose/biossíntese , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Quimiocina CXCL12/farmacologia , Proteínas Ligadas por GPI/biossíntese , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , Invasividade Neoplásica , Recidiva Local de Neoplasia/genética , PTEN Fosfo-Hidrolase/biossíntese , Fosforilação , Interferência de RNA , RNA Interferente Pequeno , Proteínas de Ligação a RNA/biossíntese , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo , Triterpenos/farmacologia
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