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1A complete sequence and comparative analysis of a SARS-associated virus(Isolate BJ01)显示文摘The genome sequence of the Severe Acute Respiratory Syndrome (SARS)-associated virus provides essential information for the identification of pathogen(s), exploration of etiology and evolution, interpretation of transmission and pathogenesis, development of diagnostics, prevention by future vaccination, and treatment by developing new drugs. We report the complete genome sequence and comparative analysis of an isolate (BJ01) of the coronavirus that has been recognized as a pathogen for SARS. The genome is 29725 nt in size and has 11 ORFs (Open Reading Frames). It is composed of a stable region encoding an RNA-dependent RNA polymerase (composed of 2 ORFs) and a variable region representing 4 CDSs (coding sequences) for viral structural genes (the S, E, M, N proteins) and 5 PUPs (putative uncharacterized proteins). Its gene order is identical to that of other known coronaviruses. The sequence alignment with all known RNA viruses places this virus as a member in the family of Coronaviridae. Thirty putative substitutions have been identified by comparative analysis of the 5 SARS- associated virus genome sequences in GenBank. Fifteen of them lead to possible amino acid changes (non-synonymous mutations) in the proteins. Three amino acid changes, with predicted alteration of physical and chemical features, have been detected in the S protein that is postulated to beinvolved in the immunoreactions between the virus and its host. Two amino acid changes have been detected in the Mprotein, which could be related to viral envelope formation. Phylogenetic analysis suggests the possibility of non-human origin of the SARS-associated viruses but provides noevidence that they are man-made. Further efforts should focus on identifying the etiology of the SARS-associated virus and ruling out conclusively the existence of otherpossible SARS-related pathogen(s).QIN E'de ZHU Qingyu YU Man FAN Baochang CHANG Guohui SI Bingyin YANG Bao PENG Wenming JIANG Tao LIU Bohua DENG Yongqiang LIU Hong ZHANG Yu WANG Cui LI Yuquan GAN Yonghua LI Xiaoyu L Fushuang TAN Gang CAO Wuchun, YANG Ruifu Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences, Beijing 100071, China WANG Jian, LI Wei, XU Zuyuan, LI Yan, WU Qingfa, LIN Wei, CHEN Weijun, TANG Lin, DENG Yajun, HAN Yujun, LI Changfeng, LEI Meng, LI Guoqing, LI Wenjie, L Hong, SHI Jianping, TONG Zongzhong, ZHANG Feng, LI Songgang, LIU Bin, LIU Siqi, DONG Wei, WANG Jun, Gane K-S Wong, YU Jun & YANG Huanming* Beijing Genomics Institute, Chinese Academy of Sciences, Beijing 101300 National Center for Genome Information, Beijing 101300, China 2003Chinese Science Bulletin2003,48,10:121
2Inhibiting effect of antisense oligonucleotides phosphorthioate on gene expression of TIMP-1 in rat liver fibrosis显示文摘AIM To observe the inhibition of antisenseoligonucleotides (asON) phosphorthioate to thetissue inhibitors metalloproteinase-1 (TIMP-1)gene and protein expression in the liver tissue ofimmunologically induced hepatic fibrosis rats.The possibility of reversing hepatic fibrosisthrough gene therapy was observed.METHODS Human serum albumin (HSA) wasused to attack rats, as hepatic fibrosis model, inwhich asONs were used to block the gene andprotein expressing TIMP-1. According to theanalysis of modulator, structure protein, codingseries of TIMP-1 genome, we designed fourdifferent asONs. These asONs were injected intothe hepatic fibrosis models through coccygealvein. The results was observed by RT-PCR formeasuring TIMP-1 mRNA expression,immunohistochemistry and in situ hybridizationfor collagen Ⅰ, Ⅲ, special staining of collagenfiber, and electron microscopic examination.RESULTS Hepatic fibrosis could last within 363days in our modified model. The expressinglevel of TIMP-1 was high during hepatic fibrosisprocess. It has been proved by theimmunohistochemical and the electronmicroscopic examination that the asONphosphorthioate of TIMP-1 could exactly expressin vivo. The effect of colchicine wasdemonstrated to inhibit the expressing level ofmRNA and the content of collagen Ⅰ, Ⅲ in theliver of experimental hepatic fibrosis rats.However, the electron microscopy research andthe pathologic grading of hepatic fibrosisshowed that there was no significant differencebetween the treatment group and the modelgroup (P>0.05).CONCLUSION The experimental rat model ofhepatic fibrosis is one of the preferable modelsto estimate the curative effect of anti-hepaticfibrosis drugs. The asON phosphorthioate ofTIMP-1 could block the gene and proteinexpression of TIMP-1 in the liver of experimentalhepatic fibrosis rats at the mRNA level. It ispossible to reverse hepatic fibrosis, and it isexpected to study a new drug of anti-hepaticfibrosis on the genetic level. Colchicine has verylimited therapeutic effect on hepatic fibrosis,furthermore, its toxicity and side effects areobvious.Qing He Nie Yong Qian Cheng Yu Mei Xie Yong Xing Zhou Yi Zhan Cao The Center of Infectious Disease Diagnosis and Treatment of PLA,Tangdu Hospital,Forth Military Medical University,Xi’an 710038,Shaanxi Province,ChinaDr,Qing He Nie graduated from Qinghai Medical College as a doctor in 1983,got master degree at Beijing 302 Army Hospital in 1993,got doctor degree at the Third Military Medical University in 1998,engaged in postdoctoral research at the Fourth Military Medical University from 1998 to 2000,now an associate professor,specialized in clinical and experimental research of infectious diseases,had more than 90 papers published,coauthor of ten books,first author of one book. 2001World Journal of Gastroenterology2001,7,3:73
3Association of H.pylori infection with gastric carcinoma:a Meta analysis显示文摘AIM: To follow the principles of evidence based medicine to reach the integrated results of these studies.METHODS: Twenty-one papers of case-control studies were selected, including 11 on gastric cancer, 7 on precancerous lesion of stomach and 3 on lymphoma of stomach: Meta analysis was used to sum up the odds ratios (OR) of these studies.RESULTS: H. Pylori vsgastric cancer (intestinal and diffuse type): the odds ratio from the fixed effect model is 3.0016(95% Cl 2.4197-3.7234, P < 0.001 ). H. Pylori vs precancerous lesion of stomach: a random effect model was used to calculate the summary odds ratio and its value is 2.5635 (95% Cl: 1.8477-3.5566, P < 0.01). H. Pylori vs lymphoma of stomach: though the quantity of literature is too small to make Meta analysis, the data of these 3 studies show that lymphoma of stomach is highly associated with H. Pylori infections.CONCLUSION: Since it had been revealed that H. Pylori infection pre-exists in gastric carcinoma and precancerous lesions, the results of Meta analysis present a strong evidence to support the conclusion that H. Pylori infection is a risk factor for gastric carcinoma.Fu-Bo Xue~1 Yong-Yong Xu~1 Yi Wan~1 Bo-Rong Pan~2 Jun Ren~2 Dai-Ming Fan~3 1 Department of Health Statistics,Department of2 Oncology3 Gastroenterology of XiJing Hospital,the Fourth Military Medical University,Xi’an 710032,Shaanxi Province,China 2001World Journal of Gastroenterology2001,7,6:66
4Expression of nuclear factor-KB in hepatocellular carcinoma and its relation with the X protein of hepatitis B virus显示文摘AIM In this study we investigated therelationship of the X protein of HBV and nuclearfactor-KB (NF-κB) and the expression of NF-KB inhuman hepatocellular carcinoma tissues.METHODS Immunohistochemistry SP methodwas used to detect the expression of NF-κB and the X protein of HBV in human hepatocellularcarcinoma tissues of 52 cases. Gene transfectionmediated by lipofectamine was used to transfectthe eukaryotic expression vector pCDNA3. 1-HBXof HBV x gene into human hepatocellularcarcinoma cell line HCC-9204 and NF-κB wasdetected.RESULTS NF-κB was widely expressed inhuman hepatocellular carcinoma tissues in atotal of 52 cases and its expression was relatedto the X protein of HBV. NF-KB was localizedboth in the cytoplasm and . The nuclei ofhepatocellular carcinoma cells in 11 cases whichwere positive for the X protein of HBV while in 41cases negative for the X protein of HBV, NF-Kbwas only localized in the cytoplasm ofhepatocellular carcinoma cells but translocatedto the nuclei of hepatocellular carcinoma cellsafter the eukaryotic expression vectorpCDNA3.1-HBX was transfected into HCC-9204cells.CONCLUSION This study strongly suggeststhat the nuclear factor NF-KB is widely expressedin hepatocellular carcinoma tissues in differentstyles according to the expression of the Xprotein of HBV. NF-κB is abnormally activated inhepatocellular carcinoma, which is probablyrelated to the X protein of HBV. The X protein ofHBV can activate NF-κB to translocate into nucleiof hepatocellular carcinoma cells.Shuang Ping Guo~1 Wen Liang Wang~1 Yu Qiang Zhai~2 Yi Ling Zhao~1 ~1Department of Pathology,Xijing Hospital of the Fourth Military Medical University,Xi’an,China ~2Department of Urology,the Central Hospital of Xi’an,China 2001World Journal of Gastroenterology2001,7,3:55
5Inhibitory effect of IGF-Ⅱ antisense RNA on malignant phenotype of hepatocellular carcinoma显示文摘INIRODUCTIONAccording to the therapeutic effect and strategy ofantisense RNA for hepatoccllular carcinoma(HCC),we have specifically synthesized partialcDNA of human insulin-like growth factor Ⅱ(IGF-Ⅱ)and constructed IGF-Ⅱ cDNA antisenseeukaryotic expression vector.The constructedvector was introduced into hepatoma cell lineSMMC-7721 to block the intrinsic IGF-Ⅱexpression.The biological behavior changes ofhepatoma cells were observed.All theseDong Hua Yang Ming Qing Zhang Jiang Du Chong Xu Oiao Ming Liang Ji Fang Mao Han Rong Qin Zi Rong Fan Department of Gastroenterology,Zhujiang Hospital,the First Military Medical University,Guangzhou 510282,China Laboratory of Molecular Biology,Zhujiang Hospital,the First Military Medical University,Guangzhou,China Departrnent of Biochemistry,the Second Military Medical University,Shanghai,China 2000World Journal of Gastroenterology2000,6,2:54
6Methodologic 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 2002World Journal of Gastroenterology2002,8,2:51
7Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma显示文摘AIM To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesisof human gastric carcinoma more directly.METHODS The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF165 complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or downregulated.RESULTS VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR,localized in both the cytoplasm and membrane.Introduction of VEGF165 antisense into human gastric cancer cells ( SGC-7901, immunofluorescence intensity,31.6%)) resulted in a significant reduction in VEGFspecific messenger RNA and total and cell surface VEGF protein ( immunofluorescence intensity, 8.9%)(P<0.05). Conversely, stable integration of VEGF165 in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity,75.4%) (P<0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tomor volume: 345.40 ± 136.31 mm3) (P<0.05 vs control SGC7901 group: 1534.40 ± 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tomor volume: 2350.50 ± 637.70mm3) (P<0.05 vs control SGC-7901 group).CONCLUSION This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer.Du-Hu Liu Xue-Yong Zhang Dai-Ming Fan Yu-Xin Huang Jin-Shan Zhang Wei-Quan Huang Yuan-Qiang Zhang Qing-Sheng Huang Wen-Yu Ma Yu-Bo Chai Ming Jin Institute of Digestive Disease,Xijing Hospital,~2 Department of Gastroenterology,Tangdu Hospital,~3Department of Histology and Embryology,~4 Department of Microbiology,~5 Department of Biochemistry,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China 2001World Journal of Gastroenterology2001,7,4:37
8Telomere erosion is independent of microsatellite instability but related to loss of heterozygosity in gastric cancer显示文摘AIM To correlate the length of the telomere to microsatellite instability (MSI) and loss of heterozygosity (LOH) of APC, MCC and DCC genes in gastric carcinomas.METHODS Telomeric restriction fragment (TRF) length of gastric cancer was measured with Southern blot. LOH of APC, MCC and DCC genes, microsatellite instability (MSI) and frameshift mutation of hMSH6, TGF-βR Ⅱ and BAX genes were analyzed by PCR-based methods.RESULTS Sixty-eight cases of sporadic gastric carcinoma were studied for MSI using five microsatellite markers. MSI in at least one locus was detected in 17 (25%) of 68 tumors analyzed. Frameshift mutations of hMSH6, TGF-βR Ⅱ and BAX were detected in 2,6 and 3 of gastric carcinomas respectively showing high MSI (≥ 2 loci, n = 8), but none was found in those showing Iow MSI (only one locus, n = 9) or MSS (tumor lacking MSI or stable, n = 51). Thirty-five cases, including all high MSI and Iow MSl, were studied for TRF. The mean TRF length was not correlated with clinicopathological parameters.No association was observed between TRF length and MSI or frameshift mutation. On the contrary, LOH at the DCC locus was related to telomere shortening (P< 0.01). This tendency was also observed in APC and MCC genes,although there was no statistical significance.CONCLUSION The development of gastric cancer can arise through two different genetic pathways. In high MSI gastric cancers, defective mismatch repair allows mutations to accumulate and generate the high MSI phenotype. In gastric cancers showing either Iow MSI or MSS, multiple deletions may represent the LOH pathway.Telomere erosion is independent of high MSI phenotype but related to the LOH pathway in gastric cancer.Dian-Chun Fang Shi-Ming Yang Xiao-Dong Zhou Dong-Xu Wang Yuan-Hui Luo Department of Gastroenterology,Southwest Hospital,Third Military Medical University,Chongqing 400038,China 2001World Journal of Gastroenterology2001,7,4:35
9Mutation analysis of APC gene in gastric cancer with microsatellite instability显示文摘AIM: To evaluate the role of APC mutation in gastric carcinogenesis and to correlate APC mutation with microsatellite instability (MSI) in gastric carcinomas. METHODS: APC mutation was measured with multiplex PCR, denaturing gradient gel electrophoresis and DNA sequencing; and MSI was analyzed by PCR-based methods.RESULTS: Sixty-eight cases of sporadic gastric carcinoma were studied for APC mutation at exon 15 and MSI. APC mutaions were detected in 15(22.1%) gastric cancers. Frequence of APC mutation (33.3 %) in intestinal type of gastric cancer was significantly higher than that in diffuse type (13.1 %, P<0.05).On the contrary, no association was observed betweerAPC mutation and tumor size,differentiation, depth of invasion, metastasis or clinical stages.Using five microsatellite markers, MSI in at least one locus was detected in 17 of 68 (25 %) of the tumors analyzed.APC mutations were all detected in MSI-L (only one locus,n=9) or MSS(tumor lacking MSI or stable, n=51), but no mutation was found in MSI-H (≥2 loci, n=8).CONCLUSION: APC mutation is involved in carcinogenesis of intestinal type of gastric cancer and is independent of MSI phenotype but related to the LOH pathway in gastric cancer.Dian-Chun Fang Yuan-Hui Luo Shi-Ming Yang Xiao-An Li Xian-Long Ling Li Fang Department of Gastroenterology,Southwest Hospital,Third Military Medical University,Chongqing 400038,China 2002World Journal of Gastroenterology2002,8,5:34
10Effect of bax,bcl-2 and bcl-xL on regulating apoptosis in tissues of normal liver and hepatocellular carcinoma显示文摘AIM: To investigate the expression of bax, bcl-2 and bcl-xL mRNA in the tissues of normal liver and hepatocellular carcinoma (HCC), and analyze the relationship between the expression of bax, bcl-2 and bcl-xL mRNA and clinical parameters of HCC patients.METHODS: The expression of bax, bcl-2 and bcl-xL mRNA of normal liver and HCC was measured by Northern blot. Statistical analyses were made by t test and correlation analysis.RESULTS: A very low mRNA level was indicated at bax,bcl-2 and bcl-xL in the HCC tissues in contrast to the tissues of normal liver by Northern blot analysis. The analyses of mRNA level revealed that HCC tissues exhibited a mean 7.6-fold decrease in bax, 4.2-fold in bcl-2 and 3.5-fold in bcl-xL in comparison with normal control tissues, respectively. Positive correlation was found between bax and bcl-xL (r=0.7061,P<0.01). There was no significance between the mRNA expression of these three genes and age, gender, tumor differentiation and tumor stage of HCC patients. CONCLUSION: The results are consistent with the fact that apoptosis rarely occurs in normal livers but increases in HCC, indicating that bcl-2 and bcl-xL may play a very important role in regulating the apoptosis of normal liver and HCC.Xiao-Zhong Guo Xiao-Dong Shao Min-Pei Liu Jian-Hua Xu Li-Nan Ren Jia-Jun Zhao Hong-Yu Li Di Wang,Department of Gastroenterology,General Hospital of Shenyang Military Region,Shenyang 110016,Liaoning Province,China 2002World Journal of Gastroenterology2002,8,6:34
11Regulation of Toll-like receptor signaling in innate immunity显示文摘Toll-like receptors sense invading pathogens by recognizing a wide variety of conserved pathogen-associated molecular patterns(PAMPs).The members of the TLR family selectively utilize adaptor proteins MyD88,TRIF,TIRAP and TRAM to activate overlapping but distinct signal transduction pathways which trigger production of different panels of mediators such as proinflammatory cytokines and type I interferon.These mediators not only control innate immunity but also direct subsequently developed adaptive immunity.TLR activation is strictly and finely regulated at multiple levels of the signal transduction pathways.AN HuaZhang,QIAN Cheng & CAO XueTao National Key Laboratory of Medical Immunology & Institute of Immunology,Second Military Medical University,Shanghai 200433,China 2010Science China(Life Sciences)2010,53,1:29
1264320例烧伤病人的分析显示文摘本文收集和分析了全军1980~1992年29个单位烧伤住院病人64320例,并与前阶段(1958~1979年)分析的16个单位48978例病人进行了对比。本阶段病人伤情虽较前阶段为重,但平均住院日明显缩短,特别有Ⅲ度者缩短达12d之多,总LA50(半数面积死亡率)及有Ⅲ度LA50分别由前阶段的75.93%和46.19%提高到96.99%和90.87%。治疗进步的主要原因,与本阶段广泛采用了早期切痂全覆盖植皮以及休克和感染的防治进步有关。另分析本阶段主要死亡原因为内脏功能不全(50.30%)、全身性感染(19.04%)和吸入性损伤(16.24%),三者占死亡总数的85%以上。为今后防治的重点。内脏功能不全中又以肺功能不全居首位,认为与吸入性损伤关系密切。Li Ao Huang Yaosheng Zhang Ning et al.(Third Military Medical College, Chongching 630038) 1995解放军医学杂志1995,20,1:29
13Endoscopic patterns of gastric mucosa and its clinicopathological significance显示文摘AIM: To explore the correlation of magnifying endoscopic patterns and histopathology, Helicobacter pylori (H pylori) infection of the gastric mucosa.METHODS: Gastric mucosal patterns in 140 patients with chronic gastritis were studied using Olympus GIF-Q240Z magnifying endoscope. Histopathological examination, rapid urease test and Warrthin-Starry staining were taken with biopsy samples from the magnified sites of stomach. The magnifying endoscopic patterns were compared with histopathological results and H pylori detection.RESULTS: The pit patterns of gastric mucosa were classified as types A (round spot), B (short rod), C (branched), D (reticular) and E (villus). The detection rate of chronic atrophic gastritis (CAG) by magnifying endoscopy was 94.3 % (33/35),which was significantly higher than that by routine endoscopy (22.9 %, 8/35) (P<0.01). The pit patterns of 31 cases of intestinal metaplasia (IM) appeared as type E in 18 cases (58.1%), type D in 8 cases (25.8 %) and type C in 5 cases (16.1%). Fourteen out of 18 patients (77.8 %) with complete type (type Ⅰ) of IM appeared as type E of pit patterns, whereas only 4 of 13 (30.8 %) patients with incomplete type (types Ⅱ and Ⅲ) of IM appeared as type E (P<0.05). Collecting venules in the anterior of lower part of gastric corpus were subgrouped into types R (regular), I (irregular) and D (disappeared).H pyloriinfection was found in 12.2 %(9/74),60 %(9/15) and 84.3 %(43/51) cases in these types respectively. H pyloriinfection rate in type R was significantly lower than that in other two types (P<0.01).CONCLUSION: Magnifying endoscopy may have an obvious value in diagnosing chronic atrophic gastritis, intestinal metaplasia and H pylori infection.Jian-Min Yang Lei Chen Yu-Lin Fan Xiang-Hong Li Xin Yu Dian-Chun Fang, Gastroenterology Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China 2003World Journal of Gastroenterology2003,9,11:28
14Hepatitis C virus infection of human hepatoma cell line 7721 in vitro显示文摘AIM To establish a cell culture system with long-term replication of hepatitis C virus in vitro.``METHODS Human hepatoma cell line 7721 was tested for its susceptibility to HCV by incubating with a serum from a patient with chronic hepatitis C. Cells and supernatant were harvested at various phases during the culturing periods The presence of HCV RNA, the expression of HCV antigens in cells and/or supernatant were examined by RT-PCR, in situ hybridization and immunohistochemistry respectively.``RESULTS The intracellular HCV RNA was first detected on d 2 after infection and then could be intermittently detected in both cells and supernatant over a period of at least three months. The expression of HCV NS3, CP10antigens could be observed in cells. The fresh cells could be infected by supematant from cultured infected cells and the transmission of viral genome from HCV-infected 7721 cells to PBMCs was also observed.``CONCLUSION The hepatoma line 7721 is not only susceptible to HCV but also supports its long-term replication in vitro.Zhi-Qiang Song~1 Fei Hao~1 Feng Min~2 Qiao-Yu Ma~2 Guo-Dong Liu~2 Department of Dermatology~1Department of Infectious Diseases~2,Southwest Hospital,Third Military Medical University,Chongqing 400038,China 2001World Journal of Gastroenterology2001,7,5:26
15Expression of insulin-like growth factor Ⅱ and its receptor in hepatocellular carcinogenesis显示文摘INTRODUCTIONInsulin-like growth factor Ⅱ(IGF-Ⅱ) is a mitogenic peptide of 74 kD and is mostly synthesized in fetal liver tissue .IGF-Ⅱ is believed to play an important role in fetal growth and development and is involved in cellular proliferation and differentiation[1-5]. Recently ,several researchers have reported increased expression of the IGF-Ⅱgene in human hepatocellular carcinoma (HCC) and adjacent non-cancerous liver tissues [6-10].Zi Rong Fan Dong Hua Yang Jun Cui Han Rong Qin Chun Chi Huang Department of Gastroenterology, Zhujiang Hospital. The First Military Medical University, Guangzhou 510282.Guangdong Province. China 2001World Journal of Gastroenterology2001,7,2:24
16Transcription factor EGR-1 inhibits growth of hepatocellular carcinoma and esophageal carcinoma cell lines显示文摘瞄准:抄写因素 EGR-1 (早生长反应 gene-1 ) 在房间生长,区别和开发起一个重要作用。它鉴别了 EGR-1 在一些瘤举办重要转变抑制活动,例如纤维肉瘤,胸癌。这个实验被设计在 hepatocellular 癌(HCC ) 和食道的癌(EC ) 的癌的过程调查 egr-1 的角色,然后在这些肿瘤细胞的生长上估价 EGR-1 的效果。方法:第一,在 HCC 和 EC 的 egr-1 的抄写和表达式,帕拉癌的纸巾和他们的正常对应物部分被检测由在 situ 杂交和免疫组织化学,与正常的人的胸和是的鼠标大脑纸巾积极控制。Egr-1 基因当时是进 HCC 的 transfected (HHCC, SMMC7721 ) 并且没有 egr-1 抄写和表示是在场的 EC (ECa109 ) 房间在线。在裸体老鼠的房间生长速度, FCM 房间周期,板克隆形成和 tumorigenicity 被观察,控制仅仅是有向量的房间线 transfected。结果:很少或没有 egr-1 抄写和表示在 HCC, EC 和正常的肝纸巾被检测。egr-1 的表示在 hepatocellular 帕拉被发现更高癌的织物(抄写水平 P=0.000;表示水平 P=0.143,可能因为在盒子的数字的少数) 并且食道的癌症的 dysplastic 织物(抄写水平 P=0.000;表示水平 P=0.001 ) 。egr-1-transfected HHCC (HCC 细胞线) 的生长率细胞和 ECa109 (EC 细胞线) 细胞比控制的慢得多。S 阶段房间,克隆形成和 tumorigenicity 的比例控制的是比这些显著地低的(减少 45.5% 在 HHCC 房间并且 34.1% 在 ECa109 房间;46.6% 和 41.8% ;80.4% 和 72.6% 分别地) 。关于上述项目 SMMC7721 (HCC ) egr-1-transfected 房间和控制之间没有明显的差别。结论:egr-1 的减少的表示可能在 HCC 和 EC 的癌的过程在正常生长的 dysregulation 起一个作用。transfected HHCC 和 ECa109 细胞的 Egr-1 基因显示出细胞生长和在 SMMC7721 (HCC 细胞线) 的恶意的显型,而是没有抑制细胞的明显的抑制。Miao-Wang Hao Li Liu,Department of Internal Medicine,Tangdu Hospital,Xi’an 710038,Shaanxi Province,China Ying-Rui Liang Ming-Yao Wu Huan-Xing Yang,Department of Pathology,Medical College of Shantou University,Shantou 515031,Guangdong Province,China Yan-Fang Liu,Department of Pathology,Fourth Military Medical University,Xi’an 710032,Shaanxi Province,China 2002World Journal of Gastroenterology2002,8,2:24
17mIL-2R,T cell subsets & hepatitis C显示文摘AIM: To study the levels of membrane interleukin-2 receptor(mIL-2R ) and T cell subsets in peripheral bloodmononuclear cells (PBMC) from patients with hepatitis Cand their role in the pathogenesis of hepatitis C.METHODS: The levels of mlL-2R and T cells subsets in PBMCWere detected by biotin- streptstividin (BSA) technique beforeand after stimulation with PHA in 203 patients with hepatitis Cwith HCV-RNA( + ), anti-HCV( + ), anti-HCV(-).RESULTS: The total expressive levels of mlL-2R before andafter stimulation with PHA(0.03 ± 0.01, 0.03 ± 0.02, 0.04 ± 0.02, 0.36±0.03), and Tcell subsets in PBMC (0.62±0.06,0.37 ± 0.05, 0.35 ± 0.07) were all lower in patients withhepatitis C than those in normal controls (0.66 ± 0.07, 0.41± 0.06, 0.31 ± 0.05, P < 0.01 ). Among the patients, thelevels of mlL-2R were lower in silence than those in situationof PHA inducting (P< 0.01). However, the levels of mlL-2Rwere similar in acute hepatitis C to that in chronic hepatitis C(P>0.05). The levels of CD3+, CD4+, CD4 +/CD8+ Were lov erand CD8 + was higher in patients with acute and chronichepatitis C with anti-HCV( + ) than those in normal controls (0.62±0.06, 0.37±0.05, 0.35±0.07, 1.18±0.30, 0.61±0.07, 0.37±0.05, 1.39±0.33, 0.31±0.05, P<0.05-P<0.01).CONCLUSION: The cellular immunity is obviously changed inpatients with hepatitis C. The levels of mlL-2R end activationof T cells am closely associated with chronicity of hepatitis C.Chao-Pin Li Ke-Xia Wang Jian Wang,Department of Aetiology and Immunology,School of Medicine,Huainan University of Technology,Huainan 232001,Anhui Province,China Bo-Rong Pan,the Fourth Military Medical University 2002World Journal of Gastroenterology2002,8,2:24
18Inhibitory effects of antisense RNA of HAb18G/CD147 on invasion of hepatocellular carcinoma cells in vitro显示文摘AIM: To study the inhibitory effects of antisense RNA of HAb18G/CD147 on invasion of hepatocellular carcinoma (HCC) cells in vitro.METHODS: Antisense RNA of HAb18G/CD147 vector PCIasHAb18G was constructed by reversely inserting HAb18G/CD147 cDNA to eukaryotic expression vector PCI-neo. The HCC cell line HHCC was transfected by PCI-asHAb18G via cation liposome. Expression of HAb18G/CD147 of transfected cells selected by G418 (geneticin) was observed by immunohistochemical SP staining and FACS (fluorescence activated cell sorting). Gelatin zymography was used to determine the effect of PCI-asHAb18G on reducing secretions of MMP2 and MMP-9 of the transfected cells. Boyden chamber was employed to test the invasion of HCC cells in vitro.RESULTS: The construction of antisense RNA vector PCIasHAb18G was verified correct by partial nucleotide sequencing and restricted endonuclease digestion. The expression of HAb18G/CD147 in transfected HHCC was inhibited by PCI-asHAb18G. Secretions of MMP-2 and MMP9 of transfected HHCC were reduced and the invasion of transfected HHCC was inhibited compared to HHCC,respectively.CONCLUSION: Invasion of HCC cells can be inhibited by antisense RNA of HAb18G/CD147. HAb18G/CD147 may be used as a potential target of drugs for anti-invasion and metastasis of HCC.Yu Li Peng Shang Ai-Rong Qian Li Wang Yong Yang Zhi-Nan Chen, Department of Cell Biology, Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China 2003World Journal of Gastroenterology2003,9,10:22
19Effect 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 2001World Journal of Gastroenterology2001,7,1:21
20Relationship between tumor necrosis factor-α and liver fibrosis显示文摘RelationshipbetweentumornecrosisfactorαandliverfibrosisWANGXin,CHENYueXiang,XUCaiFu,ZHAOGuoNing,HUANGYuXinandWANGQinLiD...WANG Xin, CHEN Yue Xiang, XU Cai Fu, ZHAO Guo Ning, HUANG Yu Xin and WANG Qin Li Department of Gastroenterology, Tangdu Hospital, The Fourth Military Medical University, Xi′an 710038, Shaanxi Province, China 1998World Journal of Gastroenterology1998,4,1:21
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