Objective To evaluate the clinical significance of radiofrequency ablation (RFA) with clustered electrodes in the treatment of unresectable large primary liver cancer. Methods Under the guidance of ultrasonography, Percutaneous and intraoperative RFA was performed in 38 patients and 5 patients,respectively. Additional ablation could be conducted if residual tumor or recurrence was found after the primary treatment. Results A total of 62 times of RFA, with a mean of 6 foci every treatment, were completed in the 43 patients, in whom the mean diameter of tumor was 7 3 cm. AFP levels had decreased to normal in 18/32 patients (56 3%) whose preoperative AFP levels were above 400 ?g/L. Postoperative CT examinations indicated that the tumor was completely ablated in 33/43 patients (76 7%). Frequent complications included fever, local pain, and liver impairment. No severe complications or treatment-related deaths were seen. The 1-year survival rate was 79 3% (23/29). Conclusions RFA with clustered electrodes in the treatment of unresectable large liver cancer can produce extensive coagulation necrosis of tumor, being a safe and effective therapeutic method. It is breaking fresh ground in the management of unresectable large

To study the value of the treatment of hepatocellular carcinoma with B ultrasonographic located radiofrequency ablation(RFA).Methods: The radiofrequency multielectrodes were inserted into the hepatic carcinoma with B ultrasonographic locating.RFA was applied with the power from 50W up to 90W. RFA scope was 1cm out of the margin of the tumor mass in three dimension. After RFA treatment, the AFP level changes and the B ultrasonography, computed tomography (CT), biopsy of the liver and hepato arterioangiography were observed.Results: One month after RFA treatment ,in those with abnormal AFP level AFP falled to normal in 18/20 patients, the volume of the tumor mass were enlarged in 9 patients, not changed in 8 patients and decreased in the others at CT and/or ultrasonography. The alive cancer cells in the margin of the tumor mass were found in 1/6 patients at biopsy. The scattering bloodstream in the carcinoma was showed in 1/8 patients on hepato arteriography. After three months, the volume of the tumor was remarkably decreased in 25 patients.Conclusion: The results suggests that RFA appears to ablate hepatic carcinoma effectively as suitable method mastered.

Objective To evaluate the treatment of postoperative bile-duct residual stones with rigid cholangioscopy. Methods Three hundred and twenty-seven cases of bile duct residual stones were treated with rigid cholangioscopy. As a route for the rigid cholangioscopy, the T-tube tract (315 cases), the U-tube tract (5 cases) and the jejunostomy tube tract of efferent limb (7 cases) were used. Results Four hundred and eighty-six rigid cholangioscopic sessions were carried out, 1.5 sessions on the average for each patient. Treatment was successful in all but one patient in whom rigid cholangioscopic access to bile duct was difficult since the T-tube tract was too long. The rate of complete removal of the stones was 95.4%. There were no serious complications. Conclusions It′s possible to pass the instrument into the common bile duct and the majority of the intrahepatic bile duct. Many of the problems associated with residual stones can be overcome by this method and good results achieved. This technique seems to be a useful new alternative in patients with difficult retained bile duct stones.

Objective To investigate the effect of prostaglandin E1(PGE1) on the expression of monocyte chemoattractant protein-1(MCP-1)in human umbilical vein endothelial cells (HUVECs) and its possible mechanism. Methods Endothelial cells were incubated with oxidized low-density lipoprotein (ox-LDL group) in the presence or absence of prostaglandin E1. The level of MCP-1 in the supernatants was determined by enzyme linked immunosorbent assay (ELISA), the expression of MCP-1 mRNA in cultured endothelial cells was detected by in-situ hybridization and the protein expression of NF-κB was analyzed by Western blot. Results Compared with ox-LDL(100 μg/ml),PGE1 markedly lowered the levels of MCP-1[(0. 327±0. 051),(0. 214±0. 213),(0. 247±0. 228)pg/ml vs. (0. 655±0. 013)pg/ml], inhibiting the expression of MCP-1 mRNA [(0. 061±0. 008), (0. 033±0. 006),(0. 026±0. 004)A/μm2 vs. (0. 220±0. 032)A/μm2] in the cultured HUVECs in a dosedependent manner (0. 001, 0. 01, 0.1 mol/L). Western blot analysis demonstrated that the amount of NF-κB p65 was attenuated after treatment with prostaglandin E1 for 24 hours. Conclusions Prostaglandin E1 can downregulate the expressions of MCP-1 and NF-κB induced by ox-LDL in HUVECs, which may thereby defend the blood vessel endothelial cell function.

Objective To determine the effect of losartan on vascular remodeling and the underlying mechanism in spontaneously hypertensive rats(SHR). Methods SHR of 12 weeks old were given losartan orally [0,15,30 mg/(kg·d),n=12]. The tail arterial pressure was measured every week.Eight weeks later, the pathological changes and p22phox expression in the thoracic aorta, the activity of catalase (CAT), the contents of H2O2 and AngⅡ in the plasma were evaluated. Results Blood pressure was increased in the SHR accompanied by the thickened wall and increased p22phox expression in the thoracic aorta. The plasma levels of H2O2 and AngⅡwere elevated while the CAT level was decreased in the SHR. Administration of losartan reversed the thickened wall and increased the CAT activity concomitantly with the decreased plasma levels of H2O2 and p22phox expression in the SHR. The plasma level of AngⅡincreased after the losartan treatment. Conclusion Oxidative stress induces the vascular remodeling of the aorta in the SHR. Losartan can reverse the vascular remodeling through down-regulating p22phox expression and inhibiting the oxidative stress.

ObjectiveTo investigate the effect of amitriptyline on lipid deposition and biochemical metabolism in a cell model of nonalcoholic fatty liver disease (NAFLD) by regulating the acid sphingomyelinase (ASM)/ceramide (CE) pathway. MethodsHepG2 and L02 cells were cultured in vitro to establish a cell model of NAFLD. MTT colorimetry was used to measure cell proliferation rate, and oil red O staining was used to observe the change of lipid droplets in cells. In the experiment, the cells were divided into normal control group, model group, Ami group, TNFα group, and Ami+TNFα group. An automatic biochemical analyzer was used to measure the levels of triglyceride (TG) and total cholesterol (TC) in cells and the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in supernatant; ELISA was used to measure the levels of CE and ASM in cells; Western blot was used to measure the protein expression ASM in cells, and RT-PCR was used to measure the mRNA expression of ASM in cells. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the Turkey test was used for further comparison between two groups. ResultsCompared with the normal control group, the NAFLD model group had significant increases in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05). Compared with the model group, the Ami group had significant reductions in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05), and the TNFα group had significant increases in the protein and mRNA expression of ASM and the levels of CE, TG, ALT, and AST (all P＜0.05). Compared with the TNFα group, the Ami+TNFα group had significant reductions in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05). ConclusionThe ASM/CE pathway promotes lipid accumulation and may lead to hepatocyte steatosis, and amitriptyline can alleviate lipid deposition in NAFLD hepatocytes by inhibiting the ASM/CE pathway.

【Objective】 To investigate the inhibitory effect of BFD-6b on colorectal cancer cell growth and its preliminary mechanism. 【Methods】 The inhibitory effect of BFD-6b on the growth of various tumor cells （SW480， MCF-7， T47D， SMMC-7721， BEL-7402， 97H， SK-HEP-1， H460， H1299， A549， MS751， and HELA） was investigated by MTT assay； the effect of BFD-6b on apoptosis and cell cycle was detected by flow cytometry； the effect of BFD-6b on the expressions of cell cycle-related proteins and apoptosis-related proteins was examined by Western blotting. 【Results】 BFD-6b inhibited the proliferation of different cancer cells such as SW480， MCF-7， H460， H1299， A549， and HELA. Among all of them， SW480 cells were most sensitive to BFD-6b， and the IC50 value was 7.09 μmol/L. Furthermore， BFD-6b could inhibit the growth of another three colorectal cell （SW620， Lovo， and HCT116 cells）； the IC50 values were 7.23， 8.08 and 8.96 μmol/L， respectively. BFD-6b could downregulate the amount of cyclinD1， cyclinE， and cell cycle-dependent kinase CDC2， thereby arresting the cell cycle at G1 phase. Also， BFD-6b downregulated the expressions of anti-apoptotic proteins Mcl-1 and Bcl-2， and upregulated the expressions of pro-apoptotic proteins BAK and BAX， thus inducing apoptosis of SW480 cells. 【Conclusion】 BFD-6b arrests SW480 cells at G1 phase by downregulating the expressions of cyclinD1， cyclinE and CDC2， and induces SW480 cell apoptosis by downregulating the expressions of Mcl-1 and Bcl-2 and upregulating the expressions of BAK and BAX， thereby inhibiting the proliferation of colorectal cancer SW480 cells.