Resection and drainage of hilar cholangiocarcinoma: an 11-year experience of a single center in mainland China.

The purpose of this study is to provide appropriate approaches for resection and drainage of hilar cholangiocarcinomas. Surgical approaches and postoperative survival rates of the patients were analyzed retrospectively. The 1-, 3-, and 5-year cumulative survival rates for patients who underwent resection were 76.6, 36.2, and 10.6 per cent, which was higher than those of 60, 14.3, and 0 per cent, respectively, in palliative operation. Moreover, the 1-, 3-, and 5-year cumulative survival rates for patients who underwent R0 were 88.9, 44.4, and 13.9 per cent, which was improved compared with those of 36.4, 9.1, and 0 per cent, respectively, in nonR0 resection. In addition, the overall survival time of patients who underwent R0 resection combined with hemihepatectomy and caudate lobe resection was longer than of those who underwent R0 without this extra operation, especially within 3 years after operation. After endoscopic metal biliary endoprothesis for patients who were intolerant of resection, liver function was improved at 2 weeks postoperation and the 1-, 3-, and 5-year cumulative survival rates for these patients were 72.7, 18.2, and 0 per cent, respectively. Treatment should be personalized. Resection is the most efficacious therapy, and negative histologic margins should be achieved in radical operation and "skeletonized" surgical operation is the basic requirement of radical treatment of hilar cholangiocarcinoma. Portal vein resection is beneficial to long-term survival and R0 resection combined with caudate lobe resection and hemihepatectomy is more efficacious for patients with Bismuth-Corlette type III hilar cholangiocarcinoma. The preferred approach of drainage in palliative operation is endoscopic metal biliary endoprothesis, which is more appropriate than tumor resection for the patients who suffer from serious comorbidities.

Reversal of adriamycin resistance of hepatocellular carcinoma by targeting it with recombined adenovirus carrying antisense multidrug resistance gene 1 RNA / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate if an adenovirus vector carrying antisense multidrug resistance gene 1 (MDR1) could reverse multidrug resistance (MDR) of HepG2/ adriamycin (ADM) cells in tumors transplanted in athymic mice.</p><p><b>METHODS</b>An adenovirus vector carrying AFP promoter and antisense MDR1 was constructed. HepG2 MDR cells (HepG2/ADM) were induced by graded resistance to ADM and were subcutaneously inoculated into athymic mice to construct the transplanted tumor. After adeno-asmdr1 was injected, the volume of the transplanted tumor and the apoptotic body in the xenograft tumor cells were observed and reverse transcriptase polymerase chain reaction was employed to investigate the expression of the mdr1-mRNA from the mouse transplanted tumor cells.</p><p><b>RESULTS</b>Following injection with adeno-asmdr1, the tumor volumes in this mice group did not increase. However the tumor volume in the PBS plus ADM group did increase significantly (P less than 0.05). In the tumor xenograft cells, mdr1 mRNA in the xenografts was assessed by RT-PCR and found to be reduced at week 1, and at week 4 in the ADM+asmdr1 group, but it was stable in the ADM group. It was only 20% in the ADM+asmdr1 group compared to the ADM group at the 4th week. Evidence of apoptosis was observed in the tumor xenograft cells treated with adeno-asmdr1, but there was rarely any apoptosis in the group treated with ADM and PBS.</p><p><b>CONCLUSION</b>Adenovirus carrying antisense mdr1 RNA can partially reverse the MDR of HepG2/ADM cells and inhibit tumor growth by down-regulating mdr1 mRNA resulting in tumor cell apoptosis.</p>

Expression of augmenter of liver regeneration in hepatic tumor cells and its clinical significance / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the effects of augmenter of liver regeneration (ALR) on the proliferation of hepatocytes and hepatic tumor cells and the expression of ALR in herpatocellular carcinoma (HCC).</p><p><b>METHODS</b>Primary rat hepatocytes, QGY and HepG2 cells were cultured separately with ALR from different species. Cell proliferation was detected by their 3H-TdR uptake. The expression of ALR was examined in 9 normal hepatic tissues and 21 HCC cases using immunohistochemistry method.</p><p><b>RESULTS</b>Different ALRs could stimulate the proliferation of HepG2 and QGY cells in a dose-dependent way in vitro, but all ALR had no influence in the proliferation of primary rat hepatocytes. The expression of ALR was absent in normal hepatic tissues, but present in all HCC hepatic tissues. However, the expression of ALR had no relationship with the differentiation and size of the carcinomas.</p><p><b>CONCLUSION</b>ALR might play an important role in the occurrence and development of HCC.</p>

The role of cyclooxygenase 2 and prostaglandin I2 in the development of portal hypertensive gastropathy / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To study the role of cyclooxygenase 2 (COX 2) and prostaglandin I2 (PGI2) in the development of portal hypertensive gastropathy (PHG).</p><p><b>METHODS</b>Forty Wistar rats were divided into surgery group (32) and control group (8). Partial portal vein ligation method was used to narrow the sectional area of portal vein to establish the experimental model of PHG in surgery group rats. Then they were divided into four groups (8 rats in each). The free pressure of portal vein was determined at the 1st, 2nd, 3rd, 4th weeks after the operation, and 8 rats were killed to observe the pathological change of gastric mucosa. The levels of 6-keto-PGF1 alpha, a stable metabolite of PGI2, were determined by radioimmunoassay in gastric mucosa homogenate and the blood of portal vein. The expression of COX 2 in gastric mucosa was determined by immunohistochemistry.</p><p><b>RESULTS</b>The free pressure of portal vein increased rapidly after partial portal vein ligation and maintained a high stable level after 1 week. They were (2.40+/-0.15) kPa, (2.38+/-0.17) kPa, (2.52+/-0.21) kPa, and (2.46+/-0.17) kPa at the 1st, 2nd, 3rd, and 4th weeks after partial portal vein ligation, while it was (0.90+/-0.16) kPa in control group (t>or=17.356, P<0.05). The gastric mucosa appeared pale, edema, hyperaemia, surface erosion, punctate hemorrhage and these lesions were more apparent with the time after the operation. The pathological examination showed that the gastric mucosa and submucosa thickened. The vessels of gastric mucosa and submucosa expanded and increased. There were lymphocytes and neutrophils infiltration around the vessels in the gastric mucosa and submucosa. The 6-keto-PGF1 alpha levels in gastric mucosa and the blood of portal vein increased rapidly and maintained a high level after partial portal vein ligation,which were higher than those in control group (104.52pg/ml+/-25.11pg/ml vs 73.62pg/ml+/- 20.33pg/ml, t=2.710, P<0.05; 180.21pg /ml+/-37.56pg /ml vs 142.11pg /ml+/-31.51pg /ml, t=2.198, P<0.05). The results of immunohistochemistry showed that the intensity and degree of the COX 2 staining in gastric tissue increased at the 1st, 2nd, 3rd, 4th weeks after partial portal vein ligation, while the COX 2 in control group rats was negative.</p><p><b>CONCLUSIONS</b>The expression of COX 2 and PGI2 in gastric tissue increased in portal hypertension. PGI2 as an inflammatory medium, damages the gastric mucosa by expanding vessels and other mechanisms in portal hypertension. It may be one of the important factors contributing to the development of PHG.</p>