Objective To enhance clinical gastrointestinal physicians’ understanding of ascites resulting from constrictive pericarditis by analyzing clinical features of. Methods A retrospective analysis was carried out in patients with constrictive pericarditis with the major presentation of ascites in our department of gastroenterology from January 1993 to May 2008. Medical records of these patients were reviewed, including data of demographics, course of desease, clinical presentation, relevant imaging studies and so on. Results There were 8 cases of constrictive pericarditis with the major presentation of ascites in our department of gastro-enterology in 15 years. The jugular varicosity was the most common manifestation in the 8 cases, followed by tabdominal distension and oedema. There were some abnormal changes in the electrocard-iography of the 8 cases. In 4 cases, no diagnosis was reached by the echocardiogram. In 8 cases,the definite diagnosis was reached by CT or MRI. Conclusion Cautions should be demanded for the patients with the major presentation of ascites in the department of gastroenterology owing to the possibility of constrictive pericarditis. In these patients, consummate physical examination is demanded such as the jugular varicosity. And the definite reason must be probed in the patients with the abnormal electrocardiographic changes.

Ascites is an important indicator of poor prognosis of liver cirrhosis.Although several guidelines and consensus statements on the management of ascites have been published in the past years,there are still a lot of controversial problems in this regard.The current contro-versial problems and difficulties in the management of ascites,such as the timing of sodium supplementation or sodium restriction,the selec-tion of diuretics,the application value of aquaretics,the strategy of albumin administration after large-volume paracentesis,and the indica-tions and efficacy of transjugular intrahepatic portosystemic shunt,are reviewed.It is pointed out that further studies on these problems with evidence-based medicine means will enhance the diagnosis and treatment of cirrhotic ascites and improve patients'prognosis.

Objective To screen the risk factors of esophageal-gastric fundus variceal bleeding,in order to provide a more economical and less invasive method for predicting esophageal-gastric fundus variceat bleeding. Methods A total of 168 diagnosed liver cirrhosis patients accompanied with ascites and 60 cases of liver cirrhosis patients with primary hepatic carcinoma were enrolled. Followed up for one year, the esophageal-gastric fundus variceal bleeding was observed and analyzed with statistic methods. Results Unconditional single factor logistic regression model analysis indicated that albumin level of ascites, serum-ascites albumin gradients (SAAG), platelets, activated partial thromboplastin time (APTT), portal vein width, length and thickness of the spleen were independent risk factors,age and serum albumin were protective factors. Multifactor analysis indicated SAAG, APTT, and portal vein width were the independent risk factors, OR was 3.559 , 2.468 and 2. 608 respectively.After building receiver operating characteristic curve, the best SAAG cut-off value was 18.50 g/L, of which the sensitivity was 96.3％ and specificity was 56.3％. Conclusion SAAG has good value in predicting esophageal-gastric fundus variceal bleeding.

Objective To investigate the effect of deoxyribonucleic acid (DNA) methylation on the expression of hepatocyte nuclear factor-4α (HNF4c) and its role in the expression of HNF4α regulated by transforming growth factor-β1 (TGF-β1).Methods The expression of HNF4αP1 mRNA in six human hepatoma cell lines (HepG2,Huh-7,Hep3B,SMMC-7721,BEL-7405 and FOCUS),20 hepatic carcinoma specimens and corresponding adjacent tissues was detected by real-time reverse transcription polymerse chain reaction (real-time RT-PCR).The methylation status of the promoter region of HNF4αP1 in six human hepatoma cell lines was examined by bisulfite sequencing PCR (BSP).FOCUS cells were treated with 5-aza-2'-deoxycytidine (5-AZA-CdR) and then the methylation status of the promoter region of HNF4αP1 was examined by BSP.The expression of HNF4αP1 mRNA was detected by real-time RT-PCR.The six human hepatoma cell lines were treated with TGFβ1 and the expression of HNF4αP1 mRNA was detected by real-time RT-PCR.FOCUS cells were cotreated with 5-AZA-CdR,TGF-β1 and 5-AZA-CdR.The expression of HNF4αP1 mRNA was detected by real-time RT-PCR,and t test was performed for statistical analysis.Results Among 20 human hepatic carcinoma specimens and corresponding adjacent tissues,the expression of HNF4αP1 mRNA of 13 human hepatic carcinoma specimens was lower than that of corresponding adjacent tissues (t=2.350,P＜0.05).The relative quantity of the expression of HNF4αP1 mRNA was higher in Hep3B,HepG2 and Huh-7 cells,whereas that in SMMC-7721,BEL-7405 and FOCUS cells was lower.The methylation of the promoter region of HNF4αP1 in HepG2,Huh-7 and Hep3B was lower,but that in SMMC-7721,BEL-7405 and FOCUS was higher.Along with the increasing of the concentration of 5-AZA-CdR (0,0.1,1.0 and 2.5 μmol/L),the degree of the methylation of the promoter region of HNF4αP1 in FOCUS cells gradually decreased (61％,46％,32％ and 27％),and however the relative quantity of the expression of HNF4αP1 mRNA gradually increased ((9.661 ± 0.336)×10-7,(2.001±0.432)×10-6,(3.689±0.714)×10-6and (4.732±2.451)×10-6).After stimulated with TGF-β1,the relative quantity of the expression of HNF4αP1 mRNA was downregulated in HepG2,Huh-7 and Hep3B cells in which the methylation of the promoter region was low (t=12.994,8.441,and 9.032,all P＜0.01).There was no significant difference in the relative quantity of the expression of HNF4αP1 mRNA in SMMC-7721,BEL-7405 and FOCUS cells in which the methylation of the promoter region was high (all P ＞ 0.05).The relative quantity of the expression of HNF4αP1 mRNA in 5-AZA-CdR treated FOCUS cells ((4.972±0.035) × 10-6) was higher than that of control group ((1.411 ± 0.104) × 10-6) and the difference was statistically significant (t=13.212,P＜0.01).The relative quantity of the expression of HNF4αP1 mRNA in FOCUS cells co-treated with 5-AZA-CdR and TGF-β1 was lower than that in cells treated with 5-AZA-CdR alone and the difference was statistically significant ((1.181 ± 0.132) × 10-6 vs (4.972 ± 0.035) × 10-6,t=13.873,P＜0.01).Conclusions The expression of HNF4αP1 is down-regulated in hepatic carcinoma tissues.DNA methylation may regulate the expression of HNF4αP1 in hepatoma cells.The methylation of HNF4αP1 promoter region inhibits the regulating function of TGF-β1 in the expression of HNF4αP1.

Portal hypertension is a common complication of chronic liver diseases and is responsible for most of the clinical consequences of cirrhosis.Accurate assessment of portal venous pressure is essential for the designing of treatment strategy and judging of prognosis.Measurement of hepatic venous pressure gradient (HVPG) is the gold standard for evaluating portal venous pressure, however, it is an invasive procedure and is hard to be performed routinely in clinical practice.Therefore, it is urgent to explore a noninvasive method for assessing portal venous pressure.Recent evidence highlights that biochemical parameters, transient elastography, CT, MRI and the conjoint analysis model of multiple parameters have the potential diagnostic value.This article reviewed the advances in study on noninvasive assessment of portal venous pressure.

Objective To improve the diagnosis and management of primary biliary cirrhosis (PBC). Methods Clincal data of 78 cases of PBC patients were reviewed. The clinical manifestations,the results of laboratory tests,and response to therapy in all the PBC patients were analysed retrospectively. Results Among 78 patients 68 were female. The mean age was 50.4?9.3years at the time when definite diagnosis was made. The major symptoms in these patients were pruritus,fatigability,and jaundice. The major signs included hepatomegaly,splenomegaly,and ascites. Very high levels of serum alkaline phosphatase (ALP) and serum gamma glutamyl transpeptidase (GGT),hyperbilirubinemia,and hypergammaglobulinemia were also detected in most of the patients. The aminotransferase levels were only slightly elevated,but the AST/ALT ratio was reversed. It took 12 months (ranging from 2 months to 10 years) to confirm the diagnosis after the onset of clinical manifestations. Ursodeoxycholic acid reduced the serum levels of ALP and bilirubin in 80% of patients and improved the symptom of pruritus and fatigability in 73.4% of patients. Conclusion PBC mainly affects middle-aged women with hepatosplenomegaly, jaundice,pruritus and fatigability as presenting features. Liver function tests typically revealed a cholestatic pattern accompanied by hypergammaglobulinemia and a positive antimitochondrial antibody (AMA) including M2 subtype (AMA-M2). Ursodeoxycholic acid could improve the abnormal liver function tests and clinical symptoms in PBC patients.

600kU/L group,10%(2/20) of patients suffering from tuberculous peritonitis were positive in the serum test,while 25%(5/20)in ascites,while in liver cirrhosis,the positive rate was 10%(2/20)in serum and 15%(3/20)in ascites.In CA 125

Objective To investigate the effect of recombinant human tumor necrosis factor (rhTNF) on telomerase activity in hepatoma cell line HepG2 cells and HepG1 6 cells. Methods TRAP ELISA method was used to determine the telomerase activity in HepG2 and HepG1 6 cells which were treated by different concentrations of rhTNF; plasmid which had been inserted 800 bp of the hTERT promoter was transiently transfected into HepG2 cells by Lipofect, and different concentrations of rhTNF were added into culture media 2 hours later, then the activity of the hTERT promoter was tested 48 hours after transfection. Results The telomerase activity of HepG2 was suppressed by rhTNF in a dose dependent manner. The expression of hTERT promoter was inhibited linearly with the dose of rhTNF within the range of 10～1 000 IU/ml. Conclusions Above results suggest that the anti tumor activity of rhTNF may attribute to its inhibitory effect on hTERT promoter expression.

Objective To investigate the effect of taurine on proliferation / apoptosis of rat hepatic stellate cells in culture and the possible mechanism involved. Methods Rat hepatic stellate cells were incubated with different concentration of taurine. Cell proliferation was assessed by MTT colorimetric assay, cell cycle and apoptosis were analysed by flow cytometry, apoptotic morphology was examined by vital staining of acridine orange, c-jun and c-fos expression was determined by immunocytochemistry and computer video text analysis system. Results Administration of 5-50 mmol/L taurine into culture medium had no toxicity to hepatic stellate cells, but could significantly inhibit hepatic stellate cell proliferation in dose-dependent manner, increase the number of cell in G 0/G 1 phase and decrease the numbers in S phase. Taurine could also markedly inhibit c-jun and c-fos expressions ( P

Objective To construct the replication deficient recombinant adenoviruses (AdHGF) of human hepatocyte growth factor (HGF) and green fluorescent protein (GFP) cDNA derived from CMV promoter using homologous recombination in bacteria provided by AdEasy system and to further investigate the effect of HGF on human fetal hepatocyte growth. Methods The HGF cDNA was obtained from the plasmid-pUCHGF by digestion, and the shuttle plasmid-pAdTrack-CMV-HGF in which the HGF cDNA was inserted into the downstream of CMV promoter was established by ligation. Then the linearized shuttle plasmid was co-transformed into bacteria with backbone vector AdEasy-1 to obtain the recombinant adenoviral plasmid-pAdHGF by homologous recombination. After packed in 293 cells, the recombinant adenoviruses-AdHGF was generated. The expression of HGF in human fetal hepatocyte was detected by RT-PCR and the effect of AdHGF on the cell cycle of fetal hepatocyte was examined by flow cytometry. Results The recombinant plasmid pAdHGF was established by homologous recombination and confirmed by restriction endonuclease digestion and sequencing. GFP expression could be observed on the third day after packing of the linearized pAdHGF in 293 cells and 4?10 10 efu/ml titer of AdHGF was obtained by CsCl gradient purification. Three days after the human fetal hepatocytes were infected by the viruses, expression of HGF in hepatocytes increased significantly and most of the hepatocytes in G 0/G 1 stages was changed to that in S and G 2/M stages.Conclusions AdHGF can be simply and rapidly generated using AdEasy system. The infection of human fetal hepatocytes by AdHGF could result in the high expression of HGF and promote the cell regeneration. AdHGF may serve as a new tool for hepatocyte transplantation and gene therapy of hepatic fibrosis.