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| 1 | HBV cccDNA in patients' sera as an indicator for HBV reactivation and an early signal of liver damage显示文摘AIM: To evaluate the covalently closed circle DNA (cccDNA)level of hepatitis B virus (HBV) in patients' liver and sera. METHODS: HBV DNA was isolated from patients' liver biopsies and sera. A sensitive real-time PCR method, which is capable of differentiation of HBV viral genomic DNA and cccDNA, was used to quantify the total HBV cccDNA. The total HBV viral DNA was quantitated by real-time PCR using a HBV diagnostic kit (PG Biotech, LTD, Shenzhen, China)described previously. RESULTS: For the first time, we measured the level of HBV DNA and cccDNA isolated from ten HBV patients' liver biopsies and sera. In the liver biopsies, cccDNA was detected from all the biopsy samples. The copy number of cccDNA ranged from from 0.03 to 173.1 per ceil, the copy number of total HBV DNA ranged from 0.08 to 3 717 per cell. The ratio of total HBV DNA to cccDNA ranged from 1 to 3 406. In the sera,cccDNA was only detected from six samples whereas HBV viral DNA was detected from all ten samples. The ratio of cccDNA to total HBV DNA ranged from 0 to 1.77%. To further investigate the reason why cccDNA could only be detected in some patients' sera, we performed longitudinal studies. The cccDNA was detected from the patients' sera with HBV reactivation but not from the patients' sera without HBV reactivation. The level of cccDNA in the sera was correlated with ALT and viral load in the HBV reactivation patients. CONCLUSION: HBV cccDNA is actively transcribed and replicated in some patients' hepatocytes, which is reflected by a high ratio of HBV total DNA vs cccDNA. Detection of cccDNA in the liver biopsy will provide an end-point for the anti-HBV therapy. The occurrence of cccDNA in the sera is an early signal of liver damage, which may be another important clinical parameter. | Johnny Sze | 2004 | World Journal of Gastroenterology2004，10，1： | 107 |
| 2 | 截短型乙型肝炎病毒表面抗原中蛋白上调c-myc基因表达的研究显示文摘目的:应用抑制性消减杂交方法构建截短型乙型肝炎病毒表面抗原中蛋白(MHBst)反式调节基因的消减文库,用免疫印迹方法验证截短型乙型肝炎病毒表面抗原中蛋白对c-myc基因的上调表达.方法:构建羧基末端截短的乙型肝炎病毒表面抗原中蛋白的真核表达载体pcDNA3.1(-)-Mt,分别以重组表达质粒pcDNA3.1(-)-Mt和空载体pcDNA3.1(-)瞬时转染HepG2细胞,提取细胞mRNA并逆转录为cDNA,用抑制性消减杂交技术,将实验组与对照组cDNA进行两次消减杂交及两次抑制性多聚酶链反应(PCR),构建cDNA消减文库,并转染大肠杆菌进行文库扩增,随机挑选克隆PCR扩增后进行测序及同源性分析.生物信息学分析结果显示部分与肿瘤发生密切相关的基因,如癌基因c-myc.结果:显示截短型乙肝病毒表面抗原中蛋白可以反式激活c-myc基因,并上调其表达.结论:成功构建截短型乙肝病毒表面抗原中蛋白反式调节基因的消减文库,细胞原癌基因c-myc是MHBst反式激活作用的靶基因,为进一步阐明乙型肝炎病毒致癌的分子生物学机制提供理论基础. | 韩萍 刘妍 成军 王刚 陆荫英 李克 李莉 | 2002 | 世界华人消化杂志2002，10，2： | 66 |
| 3 | Methodologic research on TIMP-1,TIMP-2 detection as a new diagnostic index for hepatic fibrosis and its significance显示文摘AIM: To set up a new method to detect tissue inhibitors ofmetalloproteinase1 and -2(TIMP-1 and TIMP-2) in sero ofpatients with hepatic cirrhosis, and to investigate theexpression and location of TIMP-1 and TIMP-2 in liver tissueof patients with hepatic cirrhosis, and the correlationbetween TIMPs in liver and those in sera so as to discusswhether TIMPs can be used ss a diagnosis index of hepaticfibrosisMETHODS: The monoclonal antibodies (McAbs) of TIMP-1and TIMP-2 were used to sensitize erythrocytes, and solid-phase absorption to sensitized erythrocytes (SPASE) wasused to detect TIMP-1 and TIMP-2 in the sera of patients withhepatic cirrhosis. Meanwhile, with the method of in situhybridization and immunohistochemistry, we studied themRNA expression and antigen location of TIMP-1 and TIMP-2in the livers of 40 hepatic cirrhosis patients with pathologicdiagnosis.RESULTS: With SPASE, they were 16.4 % higher in theacute hepatitis group, 33.3 % higher in the chronic hepatitisgroup, and the positive rates were 73.6 % and 61. 2 %respectively in sero of hepatic cirrhosis patients, which wereremarkably higher than those in chronic hepatitis and acutehepatitis group ( P < 0. 001 ). In 40 samples of hepaticcirrhosis tissues, all of them showed positive expression ofTIMP-1 and TIMP-2 mRNA detected withimmunohistochemistry or in situ hybridization (positive ratewas 100 % ). Expression of TIMPs in different degrees couldbe found in liver tissue with cirrhosis. TIMPs were located incytoplasm of liver cells of patients with hepatic cirrhosis.There was a significant correlation between serum TIMPslevel and liver TIMPs level.CONCLUSION: SPASE is a useful method to detect the TIMP-1 and TIMP-2 in sera of patients with hepatic cirrhosis, andTIMP-1 and TIMP-2 can be considered as a useful diagnosticindex of hepatic fibrosis, especially TIMP-1. | Oing-He Nie Yong-Oian Cheng Yu-Mei Xie Yong-Xing Zhou Bai-Xian Guang Yi-Zhan Cao,The Centre of Diagnosis and Treatment for Infectious Disease of Chinese PLA,Tangdu Hospital,Fourth Military Medical University,Xi’an 710038,Shanxi Province,China | 2002 | World Journal of Gastroenterology2002，8，2： | 51 |
| 4 | 清除乙型肝炎病毒的非细胞裂解机制显示文摘乙型肝炎病毒(HBV)的感染过程,也是机体清除HBV的过程,两者密不可分。近年来的研究表明,除了细胞裂解并清除HBV感染的机制以外,还存在清除HBV的非细胞裂解机制,而后者更具有实际应用价值,因为在达到清除HBV的目的同时,还能不损伤HBV感染的肝细胞,或者只有很轻程度的肝细胞损害。研究中发现干扰素、白介素、肿瘤坏死因子、一氧化氮以及一些未知蛋白质因子的参与,是清除HBV的非细胞裂解机制的重要因素。研究清除HBV的非细胞裂解机制,具有十分重要的实际应用前景。 | 成军 李莉 | 2002 | 世界华人消化杂志2002，10，1： | 49 |
| 5 | Expression of TIMP-1 and TIMP-2 in rats with hepatic fibrosis显示文摘AIM: To investigate the location and expression of TIMP-1 and TIMP-2 in the liver of normal and experimental hepatic fibrosis in rats. METHODS: The rat models of experimental immunity hepatic fibrosis (n=20) were prepared by the means of immunologic attacking with human serum albumin (HSA),and normal rats (n=10) served as control group. Both immunohistochemistry and in situ hybridization methods were respectively used to detect the TIMP-1 and TIMP-2 mRNA and related antigens in liver. The liver tissue was detected to find out the gene expression of TIMP-1 and TIMP-2 with RT-PCR. RESULTS: The TIMP-1 and TIMP-2 related antigens in livers of experimental group were expressed in myofibroblasts and fibroblasts (TIMP-1: 482±65 vs 60±20; TIMP-2:336±48 vs 50±19, P<0.001). This was the most obvious in portal area and fibrous septum. The positive signals were located in cytoplasm, not in nucleus. Such distribution and location were confirmed bysitu hybridization (TIMP-1/β-actin: 1.86±0.47 vs 0.36±0.08; TIMP-2/β-actin: 1.06±0.22 vs 0.36±0.08,P<0.001). The expression of TIMP-1 and TIMP-2 was seen in the liver of normal rats, but the expression level was very low. However, the expression of TIMP-1 and TIMP-2 in the liver of experimental group was obviously high. CONCLUSION: In the process of hepatic fibrosis, fibroblasts and myofibroblasts are the major cells that express TIMPs.The more serious the hepatic fibrosis is in the injured liver,the higher the level of TIMP-1 and TIMP-2 gene expression. | Qing-HeNie Guo-RongDuan Xin-DongLuo Yu-MeiXie HongLuo Yong-XingZhou Bo-RongPan | 2004 | World Journal of Gastroenterology2004，10，1： | 43 |
| 6 | Applying a highly specific and reproducible cDNA RDA method to clone garlic up-regulated genes in human gastric cancer cells显示文摘AIM: To develop and optimize cDNA representationaldifference analysis (cDNA RDA) method and to identify andclone garlic up-regulated genes in human gastric cancer(HGC) cells.METHODS: We performed cDNA RDA method by usingabundant double-stranded cDNA messages provided by twoself-constructed cDNA libraries (Allitridi-trested and paternalHGC cell line BGC823 cells cDNA libraries respectively).BamH Ⅰ and Xho I restriction sites harbored in the libraryvector were used to select representations. Northern andSlot blots analyses were employed to identify the obtaineddifference products.RESJLTS: Fragments released from the cDNA library vectorafter restriction endonuclease digestion acted as goodmarker indicating the appropriate digestion degree for libraryDNA. Two novel expressed sequence tags (ESTs) and arecombinant gene were obtained. Slot blots result showed a8-fold increase of gila-derived nexin/protease nexin 1 (GDN/PN1 ) gene expression level and 4-fold increase of hepatitis Bvirus x-interacting protein (XIP) mRNA level in BGC823 cellsafter Allitridi treatment for 72 h.CONCLUSION: Elevated levels of GDN/PN1 and XIP mRNAsinduced by Allitridi provide valuable molecular evidence forelucidating the garlic' s efficacies against neurodegenerativeand inflammatory diseases. Isolation of a recombinant geneand two novel ESTs further show cDNA RDA based on cDNAlibraries to be a powerful method with high specificity andreproducibility in cloning differentially expressed genes. | Yong Li You-Yong Lu,Beijing Institute for Cancer Research,Beijing Laboratory of Molecular Oncology,School of Oncology,Peking University,Beijing 100034,China | 2002 | World Journal of Gastroenterology2002，8，2： | 24 |
| 7 | Effect of 5-Aza-2'-deoxycytidine on the P16 tumor suppressor gene in hepatocellular carcinoma cell line HepG2显示文摘INTRODUCTIONHepatocellular carcinoma (HCC) is one of the mostcommon human malignancies worldwide[1,2], and isclosely associated with infection of HBV and HCVand contamination of aflatoxin B1[3-6]. Althoughthe molecular mechanisms of hepatocarcinogenesisremain poorly understood, an increasing number ofgenetic abnormalities have been recognized[7-10],for example, the p16 gene[11,12] the p53gene[13-18], the E-cadherin gene[19], and the c-mycgene[20]. | Li Hua Liu1 Wen Hua Xiao2 Wei Wen Liu3 1Department of Oncology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China (now working in Department of Gastroenterology, General Hospital of PLA, Lanzhou 730050, Gansu Province, China)2Department of Oncology3Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China | 2001 | World Journal of Gastroenterology2001，7，1： | 21 |
| 8 | The point mutation of p53 gene exon7 in hepatocellular carcinoma from Anhui Province,a non HCC prevalent area in China显示文摘AIM:In hepatocellular carcinoma(HCC)prevalent areas of China,the point mutation of p53 exon7 is highly correlated with hepatitis B virus(HBV)infection and aflatoxin B intake While in non-HCC_prevalent areas of China,these factors are not so important in the etiology of HCC.Therefore,the point mutation of p53 exon7 may also be different than that in HCC-pervalent areas of China.The aim of this study is to investigate the status and carcinogenic role of the point mutation of p53 gene exon7 in hepatocellular carcinoma from Anhui Province,a non-HCC-prevalent area in China.METHODS:RCR,PCR-SSCP and PCR-RFLP were applied to analyze the homozygous deletion and point mutation of p53 exon7 in HCC samples from Anhui,which were confimed by DNA sequencing and Genbak comparison.RESULTS:In the 38 samples of hepatocellular carcinoma,no homozygous deletion of p53 exon7 was detected and point mutations of p53 exon7 were found in 4 cases,which were found to be heterozygous mutation of codon 249 with a mutation rate of 10.53%(4/38).The third base mutation(G→T)of p53 codon 249 was found by DNA sequencing and Genbank comparison.CONCLUSION:The incidence of point mutation of p53 codon 249 is lower in hepatocellular carcinoma and the heterozygous mutation of p53 exon7 found in these patients only indicate that they have genetic susceptibility to HCC p53 codon 249 is a hotspot of p53 exon7 point mutation suggesting that the point mutation of p53 exon 7 may not play a majuor role in the carcinogenesis of HCC in Anhui Province,a non-HCC-prevalent area in China. | LiuH WangY 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 13 |
| 9 | 胸腺肽α1对慢性乙型肝炎患者免疫系统的影响显示文摘目的:了解胸腺肽α 1(Tα1)对慢性乙型肝炎患者免疫系统的影响,评价Tα1对慢性乙型病毒性肝炎的疗效。方法:选择60例慢性乙型肝炎患者,其中Tα1组25例,给予Tα1(1.6mg,sc,2次/wk,3-6 mo)治疗,联合组35例,给予Tα1联合贺普丁(0.1g,po,1次/d,3-6 mo)治疗,另选60例作为对照组,仅给予保肝治疗。应用双抗体酶联分析法检测治疗前后血清中IFN-γ和IL-4的浓度,以IFN-γ代表Th1,IL-4代表Th2,从而计算Th1/Th2比值;采用流式细胞仪观察外周血CD_4^+T,CD_s^+T细胞亚群。结果:联合组与对照组比,治疗后肝功能改善显著(P<0.01);联合组乙型肝炎病毒标志物HBsAg或HBeAg阴转(9例)及HBV-DNA定量指标降低(14例),与对照组比,均具有统计学差异(P<0.01;P<0.05).但Tα1组分别与对照组、联合组比,无统计学差异(P>0.05)。Tα1组治疗后CD_4^+T细胞增高(由31.3±2.4增高到36.1±2.5)具有统计学意义(P<0.01),CD_8^+T细胞稍高且CD4^+/CD8^+无明显变化,相差无统计学意义(P>0.05);IFN-γ浓度(由71.3±21.0增高到83.7±21.4)及Th1/Th2比值升高(由0.79±0.2增高到0.98±0.3)均有统计学意义(P均<0.05),但IL-4表达水平变化无统计学意义。结论:Tα1能提高机体的细胞免疫功能,有利于病毒清除和疾病的恢复。 | 段国荣 聂青和 周永兴 王全楚 田长印 刘拉羊 薛红安 | 2003 | 世界华人消化杂志2003，11，6： | 12 |
| 10 | Rapid screening mitochondrial DNA mutation by using denaturing high-performance liquid chromatography显示文摘AIM:To optimize conditions of DHPLC and analyze the effectiveness of various DNA polymerases on DHPLC resolution,and evaluate the sensitivity of DHPLC in the mutation screening of mitochondrial DNA(mtDNA).METHODS:Two fragments of 16s gene of mitochondrial DNA(one of them F2 is a mutant fragment) and an A3243G mutated fragment were used to analyze the UV detection limit and determine the minimum percentage of mutant PCR products for HDPLC and evaluate effcets of DNA polymerases on resolution of DHPLC.Under the optimal conditions.we analyzed the mtDNA mutations from muscle tissues of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes(MELAS) and screened blindly for variances in D-loop region of mtDNA from human gastric tumor specimen.RESULTS:Teh A3243G variants were detected in 12 cases of MELAS,no alterations were detected in controls and these results were consistent with the results obtained by analysis of RFLP with APal.We also identified 26 D-loop variances in 46 cases of human gastric cancer tissues and 38 alterations in 13 gastric cancer cell lines.The mutation of mtDNA at 80ng PCR products containing a minimum of 5% mutant sequences could be detected by using DHPLC with UV detector Moreover,Ampli-Taq Gold polymerase was equally as good as the proofreading DNA polymerase(e.g.Pfu)in eliminating the false positive produced by Tay DNA polymerases.CONCLUSION:DHPLC is a powerful,rapid and sensitive mutaion screening method for mtDNA.Proofreading DNA Ploymerase in more suitalbe for HDPLC analysis than Taq polymerase. | LinMR PanKF 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 11 |
| 11 | The analysis of γ-glutamyl transpeptidase gene in different type liver tissues显示文摘AIM: To probe the value of γ-glutamyl transpeptidase (GGT)messenger RNA in monitoring canceration of liver cells andfor early diagnosis of hepatocellular carcinoma (HCC), byresearching the types of GGT messenger RNA (GGTmRNA)in liver tissues and peripheral blood of different hepatopathy.METHODS: The three types of GGTmRNA (A, B, C) in livertissues and peripheral blood from the patients with HCC,noncancerous hepatopathy, hepatic benign tumor, secondarycarcinoma of liver, and healthy persons were detected byreverse-transcription polymerase chain reaction (RT-PCR).RESULTS: (1) In normal liver tissues, type A waspredominantly found (100.00 %), type B was not found,type C was found occasionally (25.00 %). (2) The distributionof types of GGTmRNA in liver tissues with acute hepatitis,chronic hepatitis, cirrhosis, alcoholic hepatopathy was similaras in normal liver tissues (P>0.05), but type B was found in3 of 18 patients with chronic hepatitis (16.67 %), and alsoin 3 of 11 patients with cirrhosis (27.27 %). (3) There wasno significant difference of types of GGTmRNA between livertissues with hepatic benign tumor, secondary carcinoma ofliver and normal liver tissues (P>0.05). (4) Type B waspredominant in cancerous tissues with HCC (87.5 %), theprevalence of type B in cancerous tissues was significantlyhigher than that in normal liver tissues (0/12) (P<0.05), butthe prevalence of type A in cancerous tissues (46.88 %)was significantly lower than that in normal liver tissues(100.00 %) (P<0.05), and the prevalence of type C (6.25 %)in cancerous was the same as that in normal liver tissues(25.00 %) (P>0.05). In noncancerous tissues of livers withHCC, the main types were type A and type B, the prevalenceof type A (85.71%, 90.48 %) and type C (14.29 %, 9.52 %)in noncancerous tissues of liver with HCC was similar asthat in normal liver tissues (A: 100.00 %; C: 25.00 %)(P>0.05), but the prevalence of type B (80.95 %, 76.19 %)in noncancerous tissues of livers with HCC was significantlyhigher than that in normal liver tissues (0/12) (P<0.05). (5)The prevalence of type B (37.5 %) in peripheral blood withHCC was higher than that in normal person (0/12) (P<0.05).In peripheral blood, type B was found in 4 of 11 cases ofHCC with serum AFP negative.CONCLUSION: The shift of types of GGTmRNA from A toB in liver tissues may be closely related to the developmentof HCC, and the analysis of GGT gene may provide a usefultool for early diagnosis of HCC. | Guo-Qing Han Cheng-Yong Qin Rong-Hua Shu The Center of Liver Diseases, Shandong Provincial Hospital, Clinical Medical College of Shandong University, Jinan 250021, China | 2003 | World Journal of Gastroenterology2003，9，2： | 11 |
| 12 | Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization显示文摘AIM: To investigate the presence of H. pylori DNA withingastric epithelial cells in patients with H. pylori infection andits possible carcinogenic mechanism.METHODS: Total 112 patients, with pathologically confirmedchronic superficial gastritis, chronic atrophic gastritis,intestinal metaplasia, atypical hyperplasia or gastrio cancerwere studied .Among them, 28 were H. pylori negative and84 H. pylori positive. H. pylori DNA in gastric epithelialcells was detected by GenPoint catalyzed signalamplification system for in situ hybridization.RESULTS: In the H. pylori positive group, zero out of 24chronic superficial gastritis (0. 0 %), four out of 25precancerous changes (16.0 %) and thirteen out of 35gastric cancers (37. 1 %) showed H. pylori DNA in thenucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells wereprogressively inoreased in chronic superficial gastritis,precancerous changes and gastric cancer groups (χ2 = 12.56, P = 0. 002); One out of 24 ohronic superficial gastritis(4.2 %), eleven out of 25 precancerous ohangas (44.0 %)and thirteen out of 35 gastric cancers (37. 1 %) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (χ2 =10.86, P = 0.004). In the H. pylorinegative group, only onepatient with gastric cancer was found H. pylori DNA in thenucleus of gastric epithelial cells; Only two patients, onepatient with precancerous changes and another with gastriccancer, showed H. pylori DNA in the cytoplasm of gastricepithelial calls. Furthermore, H. pylori DNA must have been inthe ayteplasm as long as it existed in the nucleus of gastricepithelial cells.CONCLUSION: H. pyloriDNA exists both in the nucleus andthe cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronicsuperficial gastritis, precancerous changes to gastric canceris associated with higher positive rates of H. pylori DNApresence in the nucleus of gastric epithelial cells. | Xin-Liang Lu Ke-Da Oian Xun-Qiu Tang Yong-Liang Zhu Qin Du,Department of Digestive Diseases,Second Affiliated Hospital,Zhejiang University Medical College,Hangzhou 310009,Zhejiang Province,China | 2002 | World Journal of Gastroenterology2002，8，2： | 11 |
| 13 | 干扰素联合胸腺肽治疗慢性乙型肝炎显示文摘目的评价IFN-α联合胸腺肽治疗慢性乙型肝炎(CHB)的疗效和安全性,探讨两者联合治疗的协同作用。方法 HBV DNA及HBeAg阳性的CHB患者215例,随机分为A,B两组。A组采用IFN-α和胸腺肽联合治疗,IFN-α3~5MU,1次·d^1im,15d后改为隔日一次im;胸腺肽100mg,1次·d^1静滴,1mo后改为20mg,1次·d^1im,疗程6mo,B组单用IEN-α,疗程6mo治疗结束后随访6mo,观察两组肝功能和乙肝病毒标志(HBVM及HBV DNA)的变化情况和不良反应。结果治疗结束时,两组临床症状均明显改善,A组中81例(63.3%)ALT恢复正常,而B组仅43例(49.4%)正常,两组有显著性差异(P<0.05);A组有70%HBV DNA阴转,59.4%HBeAg阴转,56.3%为近期完全应答(ALT复常,HBV DNA及HBeAg均阴转),B组分别为63.2%,48.3%和46.0%,两组无显著性差异(P>0.05)治疗结束后6mo,A组有65.6%ALT复常,68.8%HBV DNA阴转,66.4%HBeAg阴转,62.5%为持续完全应答;而B组则分别为31.0%,40.2%,37.9%和27.6%,两组有非常显著性差异(P<0.01)。治疗结束时已产生生化学和(或)病毒学应答的病例,随访期间A组有22.2%ALT又异常,23.3%HBV DNA再转阳,13.2%HBeAg再转阳,B组则分别为44.2%,41.8%和31.0%,B组生化学和病毒学复发率显著高于A组,具有显著性差异(P<0.05),治疗结束时无应答的病例中,随访期间A组有44.7%ALT复常,50% HBV DNA阴转,36.5% HBeAg阴转,而B组分别为6.8%,9.4%和8.9%,A组的生化学和病毒学滞后应答率显著高于B组,两组具有非常显著性差异(P均<0.01),治疗过程中,A组除出现与IFN-α治疗相关的初期副反应外,未发现其他副作用。结论 IFN-α与胸腺肽联合治疗CHB具有明显的协同作用,可明显改善肝功能,抗病毒效果好,明显优于单用IFN-α组,大大提高了IFN-α的远期疗效,使复发率明显降低,是CHB患者安全、有效的治疗方法,当然,62.5%的持续应答率远非理想效果,需要继续探索新的联合治疗方案。 | 游晶 庄林 唐宝璋 扬惠 扬微波 李武 张宏丽 张艳梅 张禄 严绍明 | 2001 | 世界华人消化杂志2001，9，4： | 9 |
| 14 | Expression of liver cancer associated gene HCCA3显示文摘AIM: To study and clone a novel liver cancer reisted gene,and to explore the molecular basis of liver cancer genesis.METHODS: Using mRNA differential display polymerasechain reaction (DDPCR), we investigated the difference of mRNA in human hepatocellular carcinoma (HCC) and paired surrounding liver tissues, and got a gene probe. By screening a human placenta cDNA library and genomic homologous extend, we obtained a full-length cDNA named HCCA3. We analyzed the expression of this novel gene in 42pairs of HCC and the surrounding liver tissues, and distribution in human normal tissues by means of Northern blot assay.RESULTS: A full-length cDNA of liver cancer associated gene HCCA3 has been submitted to the GeneBank nucleotide sequence databases ( Accession No. AF276707 ). The positive expression rate of this gene was 78.6% (33/42) in HCC tissues, and the clinical pathological data showed that the HCCA3 was closely associated with the invasion of tumor capsule ( P = 0.023) and adjacant small metastasis satellite nodules lesions ( P= 0.041). The HCCA3 was widely distributed in the human normal tissues, which was intensively expressed in lungs, brain and colon tissues,while lowly expressed in the liver tissues.CONCLUSION: A novel full-length cDNA was cloned and differentiated, which was highly expressed in liver cancer tissues. The high expression was closely related to the tumor invasiveness and metastasis, that may be the late heredited change in HCC genesis. | Zheng-Xu Wang~1 Gui-Fang Hu~1 Hong-Yang Wang~2 Meng-Chao Wu~2 1 Department of General Surgery,Chinese PEA General Hospital of Lanzhou Military Command,Lanzhou 730050,Gansu Province,China2 Eastern Hepatobilliary Surgical Hospital,Second Military Medical University,Shanghai 200438,China | 2001 | World Journal of Gastroenterology2001，7，6： | 9 |
| 15 | Signal transduction of gap junctional genes,connexin32,connexin43 in human hepatocarcinogenesis显示文摘AIM: To investigate gap junctional intercellular communication (GJIC) in hepatocellular carcinoma cell lines, and signal transduction mechanism of gap junction genes connexin32(cx32),connexin43(cx43) in human hepatocarcinogenesis.METHODS: Scarped loading and dye transfer (SLDT) was employed with Lucifer Yellow (LY) to detect GJIC function in hepatocellular carcinoma cell lines HHCC, SMMC-7721and normal control liver cell line QZG. After Fluo-3AM loading, laser scanning confocal microscope (LSCM) was used to measure concentrations of intracellular calcium [Ca2+]i in the cells. The phosphorylation on tyrosine of connexin proteins was examined by immunoblot.RESULTS: SLDT showed that ability of GJIC function was higher in QZG cell than that in HHCC and SMMC-7721 cell lines. By laser scanning confocal microscopy, concentrations of intracellular free calcium [Ca2+]i was much higher in QZG cell line (108.37 nmol/L) than those in HHCC (35.13nmol/L) and SMMC-7721 (47.08 nmol/L) cells. Western blot suggested that only QZG cells had unphosphorylated tyrosine in Cx32 protein of 32 ku and Cx43 protein of 43ku; SMMC-7721 cells showed phosphorylated tyrosine Cx43 protein.CONCLUSION: The results indicated that carcinogenesis and development of human hepatocellular carcinoma related with the abnormal expression of cx genes and disorder of its signal transduction pathway, such as decrease of [Ca2+]i,post-translation phosphorylation on tyrosine of Cx proteins which led to a dramatic disruption of GJIC. | Xiang-DongMa XingMa Yan-FangSui Weng-LiangWang Chun-MeiWang | 2003 | World Journal of Gastroenterology2003，9，5： | 8 |
| 16 | 肝癌组织HSP70和caspase 3的表达意义显示文摘目的:研究热休克蛋白70和caspase 3在肝细胞癌及癌旁肝组织中的表达及其临床意义. 方法:利用免疫组织化学检测70例肝细胞癌及其癌旁肝组织中HSP70和caspase 3蛋白的表达. 结果:HCC中HSP70的阳性率和阳性强度明显高于癌旁肝组织(68.6%VS 31.4%,P<0.01),而caspase3蛋白的阳性率和阳性强度明显低于癌旁肝组织(17.1%vs 35.7%,P<0.01). 在HCC中HSP70和caspase3蛋白的表达强度与HCC的分化程度和肿瘤的大小明显相关,分化愈差和肿瘤愈大HSP70表达愈强(分别为:F=5.219和5.421,P均<0.01)而caspase3蛋白表达愈弱(分别为F=5.944和4.571,P均<0.01). 统计学分析显示在HCC及其癌旁肝组织中HSP70和caspase 3蛋白的表达呈明显负相关(分别为:r=0.4126和-0.5237,P均<0.01). 结论:本文结果提示在HCC发生过程中HSP70的表达可能通过促进细胞的转化和增生及抑制细胞的凋亡,使HCC呈现无限制的生长及恶性程度不断增高;检测HSP70有望能成为判断HCC预后的重要指标之一. | 彭绍华 邓虹 冯德云 郑晖 | 2004 | 世界华人消化杂志2004，12，4： | 8 |
| 17 | 早期肠道营养对烧伤大鼠肠粘膜损伤和修复的影响显示文摘目的研究早期肠道营养对烧伤大鼠肠粘膜损伤和修复的影响及其可能的机制.方法采用30%体表面积Ⅲ度烧伤大鼠模型,随机分成伤前对照(C),静脉营养(PN)及肠道营养(EN)组,EN 和 PN 组给予等氮、等热卡、等体积的营养液.在此基础上动态观察了肠组织中肠三叶因子(ITF)含量、血浆二氨氧化酶(DAO)活性、肠粘膜跨膜电位差(PD)及增殖细胞核抗原(PCNA)的变化,并进行相关分析.结果烧伤后肠粘膜组织结构受损,血浆 DAO 活性明显增高,从伤前的0.32±0.02(10~3U·L^(-1))增为1.23±0.53(10~3U·L^(-1)),相差显著(P<0.01).而 PD,PCNA 值及 ITF 含量分别从伤前的13.53±0.41(mV),823.46±240.56(A),369±65(ng·g^(-1))降至伤后的5.27±0.17(mV),247.39±112.23(A)和15±4(ng·g^(-1)),相差显著(P<0.05~0.01).两组相比EN 组大鼠肠道受损程度明显低于 PN 组,同时其 ITF 含量、PD,PCNA 值均高于 PN 组[EN组分别为129±46(ng·g^(-1)),6.02±0.17(mV)和612.66±188,27(A)而 PN 组分别为15±4(ng·g^(-1)),5.27±0.17(mV)和247.39±112.23(A)];而 EN 组大鼠血浆 DAO 活性为0.61±0.14(10~3U·L^(-1))显著低于 PN 组的0.90±0.16(10~3U·L^(-1))(P<0.01).相关分析显示,ITF 含量同血浆 DAO 活性呈显著负相关(r_1=-0.964,P<0.01),而同 PCNA 及 PD 值呈显著正相关(r_2=0.884,P<0.05;r_3=0.983.P<0.01).结论严重烧伤后肠粘膜结构受损与肠道合成和分泌 ITF 的能力大幅下降有关,肠道营养可降低伤后 ITF 下降的幅度可能是其在减轻肠粘膜损伤,促进肠粘膜修复方面优于静脉营养的重要原因. | 彭曦 颜洪 陶麟辉 赵云 王裴 汪仕良 | 2000 | 世界华人消化杂志2000，8，11： | 8 |
| 18 | 乙型肝炎病毒核心启动子的结构及调节研究显示文摘0引言
乙型肝炎是一种严重威胁人类健康的疾病,呈全球性分布,目前全世界有3.5亿人感染乙型肝炎病毒(HBV),其中相当一部分感染者发展为慢性肝炎,少数还发展为肝硬化甚至肝癌,至今仍缺乏有效控制[1-5].造成这一局面的原因很多,其中关于HBV与肝细胞之间相互作用的分子生物学机制的研究进展相对滞后是严重影响新型治疗技术和新型药物开发与研究的重要原因之一.进一步弄清HBV DNA的复制、转录及调节的过程,对于我们研究乙型肝炎的发病机制具有重要意义.本文仅就乙型肝炎病毒核心启动子(CP)结构及调节近几年的研究进展作一综述. | 杨艳杰 成军 陈东风 刘妍 杨倩 王建军 | 2003 | 世界华人消化杂志2003，11，7： | 7 |
| 19 | 羧基末端截短型乙型肝炎病毒表面抗原中蛋白反式激活作用的研究显示文摘0引言
乙型肝炎病毒(HBV)的感染,不仅引起急、慢性病毒性肝炎,而且与肝纤维化、肝细胞癌的发生、发展过程密切相关[1-5]. | 成军 刘妍 洪源 王建军 杨倩 | 2003 | 世界华人消化杂志2003，11，8： | 7 |
| 20 | 乙型肝炎病毒X基因启动子结构及调节研究显示文摘0引言
乙型肝炎病毒(HBV)持续感染导致全球性健康问题,目前全世界有3.5亿人感染HBV,约占全部人口的6%.其中相当一部分感染者发展为慢性肝炎,少数还发展为肝硬化甚至肝细胞癌(HCC),至今仍缺乏有效控制[1-4]. | 邵清 成军 白雪帆 | 2003 | 世界华人消化杂志2003，11，8： | 6 |
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