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| 1 | 肝硬化腹水病人的处理—美国肝病学会实践指南相关问答显示文摘 | 郝建宇 杨立新 | 2007 | 中国实用内科杂志2007，27，8： | 51 |
| 2 | 肝硬化腹水的诊断与治疗进展显示文摘 | 王贵强 刘卫平 | 2006 | 中国实用内科杂志2006，26，11： | 27 |
| 3 | Alpha-fetoprotein stimulated the expression of some oncogenes in human hepatocellular carcinoma Bel 7402 cells显示文摘AIM:To investigate the molecular mechanism of alphafetoprotein (AFP) on regulating the proliferation of human hepatocellular carcinoma cells.METHODS: Alpha-fetoprotein purified from human umbilical blood was added to cultured human hepatocellular carcinoma Bel 7402 cells in vitro for various treatment periods. The expression of c-fos, c-jun,and N-ras mRNA involved in proliferation and differentiation of cells was analyzed by Northern blot,and the expression of mutative p53 and p21^ras proteins was determined by Western blot.RESULTS:The results showed that AFP (20mg/L) stimulated mRNA expression of these oncogenes in Bel 7402 cells.The expression of c-fos mRNA increased by 51.1%,60.9%,96.0%,and 25.5% at 2, 6, 12, and 24 h, respectively.The expression of c-jun and N-ras mRNA reached to the maximum which increased by 81.3% and 59.9% as compared with the control alter 6h and 24h incubation with AFP, respectively.Western blot assay also demonstrated that AFP promoted the expression of mutative p53 and p21^ras proteins, and the increased rate of those proteins was 13.0%,39.9%, and 70.9%, as well as 35.2%, 102.6%, and 46.8% at 6, 12, and 24h,respectively, as compared with the control.Both human serum albumin (the same dosage as AFP) and monoclonal anti-AFP antibody failed to stimulate the expression of these oncogenes,but anti-AFP antibody could block the functions of AFP.CONCLUSION:The data indicate that AFP can stimulate the expression of some oncogenes to enhance the proliferation of human hepatocellular carcinoma Bel 7402 cells. | Meng-SenLi Ping-FengLi QianChen Guo-GuangDu GangLi | 2004 | World Journal of Gastroenterology2004，10，6： | 19 |
| 4 | Therapeutic polypeptides based on HBcAg_(18-27) CTL epitope can induce antigen-specific CD_8^+ CTL-mediated cytotoxicity in HLA-A2 transgenic mice显示文摘To explore how to bigger an HLAI-restricted CD8+ T cellresponse to exogenously synthesized polypeptides in vivo. | Tong-DongShi Yu-ZhangWu Zheng-CaiJia WeiZhou Li-YunZou | 2004 | World Journal of Gastroenterology2004，10，8： | 17 |
| 5 | Effect of arsenic trioxide on rat hepatocarcinoma and its renal cytotoxicity显示文摘AIM: To study the effect of arsenic trioxide (As2O3) on rat experimental hepatocarcinoma and its renal cytotoxicity.METHODS: The hepatocarcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks.Before the treatment, the rat models were randomly divided into 5 groups. In the treatment groups, three doses of As2O3 were injected into rat abdominal cavity, the total time of drug administration was 4 weeks. Cisplatin control or the blank group was injected into abdominal cavity with equal amount of cisplatin or saline at the same time,respectively. On the 7th, 14th and 28th day after the treatment, the hepatocarcinoma nodules were obtained and the morphologic changes of hepatocarcinoma cells were observed under light and electron microscopes;Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocarcinoma tissues; flow cytometry (TUNEL assay)was used to detect the apoptosis of liver cancer cells and the change of cytokinetics. On the 28th day, the kidneys were obtained and their histologic changes were observed under light microscope, and immunohistochemistry (SP stain) was also employed to detect the expression of bcl-2and PCNA. Cisplatin and saline solution were used as the control.RESULTS: As2O3 could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes.The incidence of apoptosis of hapatocarcinoma cells was elevated (P=0.001). The elevation was the most higher in the group of middle-dose of As2O3 (1 mg.kg-1), significantly higher than that of the other arsenic groups and the controls (P=0.001). Large dose of As2O3 (5 mg.kg-1) was able to arise the incidence of apoptosis, but also produced a large amount of necrosis and inflammatory reaction. Middle dose of As2O3 dramatically increased the cell number in G2/M phase (P=0.0001), and apoptosis happened apparently.The expression of bcl-2 and bax was related to the dose of As2O3. With the up-regulation of apoptotic incidence, the ratio of bcl-2/bak decreased. But the incidence of apoptosis was not the highest status and the ratio of bcl-2/bax was at the lowest when the highest-dose of As2O3 was used.There was significant difference among the PCNA indexes (PCNA L1) of the five groups. Of them, three arsenic groups all showed decrease of different degrees, and this downregulation was most obvious in group A. There was significant difference among the three groups (P=0.016).Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013).In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA L1. But in the group of cisplatin,the PCNA L1 increased significantly (P=0.001).CONCLUSION: AS2O3 can induce apoptosis of rat hepatocellular carcinoma cells. And there is optimum dose;too high dose will induce the cytotoxic effect, while certain dose of As2O3 is able to block the cell cycle at G2/M phase.As2O3 had the most remarkable influence on G2/M cells,and it can also induce apoptosis to cells at other phases.As2O3 can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner.Compared with cisplatin, As2O3 didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects. | Shao-Shan Wang Ti Zhang Xi-Lu Wang Li Hong Department of Surgery of Dagang Hospital 300270,Tianjin,China Qing-Hui Qi Department of Chinese and Western Integral Surgery of Master Hospital of Tianjin Medical University 300052,Tianjin,China | 2003 | World Journal of Gastroenterology2003，9，5： | 17 |
| 6 | 肝肾综合征的诊断、分型和治疗进展显示文摘 | 章友康 | 2006 | 中国实用内科杂志2006，26，3： | 16 |
| 7 | Expression of growth hormone receptor and its mRNA in hepatic cirrhosis显示文摘AIM: To investigate the expression of growth hormone receptor (GHR) and mRNA of GHR in cirrhotic livers of rats with the intension to find the basis for application of recombinant human growth hormone (rhGH) to patients with liver cirrhosis.METHODS: Hepatic cirrhosis was induced in SpragueDawley rats by administration of thioacetamide intraperitoneally for 9-12 weeks. Collagenase Ⅳ was perfused in situ for isolation of hepatocytes. The expression of GHR and its mRNA in cirrhotic livers was studied with radio-ligand binding assay, RT-PCR and digital image analysis.RESULTS: One class of specific growth hormone-binding site, GHR, was detected in hepatocytes and hepatic tissue of cirrhotic livers. The binding capacity of GHR (RT, fmol/mg protein) in rat cirrhotic liver tissue (30.8±1.9) was significantly lower than that in normal control (74.9±3.9) at the time point of the ninth week after initiation of induction of cirrhosis (n=10, P<0.05), and it decreased gradually along with the accumulation of collagen in the process of formation and development of liver cirrhosis (P<0.05). The number of binding sites (×10 4/cell) of GHR on rat cirrhotic hepatocytes (0.86±0.16) was significantly lower than that (1.28±0.24)in control (n= 10, P<0.05). The binding affinity of GHR among liver tissue, hepatocytes of various groups had no significant difference (P>0.05). The expression of GHR mRNA (riOD,pixel) in rat cirrhotic hepatic tissues (23.3±3.1) was also significantly lower than that (29.3±3.4) in normal control (n=10, P<0.05).CONCLUSION: The growth hormone receptor was expressed in a reduced level in liver tissue of cirrhotic rats,and lesser expression of growth hormone receptors was found in a later stage of cirrhosis. The reduced expression of growth hormone receptor was partly due to its decreased expression on cirrhotic hepatocytes and the reduced expression of its mRNA in cirrhotic liver tissue. | Hong-TaoWang ShuangChen JieWang Qing-JiaOu ChaoLiu Shu-SenZheng Mei-HaiDeng Xiao-PingLiu | 2003 | World Journal of Gastroenterology2003，9，4： | 14 |
| 8 | Therapeutic polypeptides based on HBV core 18-27 epitope can induce CD_8^+ CTL-mediated cytotoxicity in HLA-A2^+ human PBMCs显示文摘AIM: To explore how to improve the immunogenicity of HBcAg CTL epitope based polypeptides and to trigger an HBV-specific HLA I-restricted CD8^+ T cell response in vitro.METHODS: A new panel of mimetic therapeutic peptides based on the immunodominant B cell epitope of HBV PreS2 18-24 region, the CTL epitope of HBcAg18-27 and the universal T helper epitope of tetanus toxoid (TT) 830-843 was designed using computerized molecular design method and synthesized by Merrifield's solid-phase peptide synthesis.Their immunological properties of stimulating activation and proliferation of lymphocytes, of inducing TN1 polarization,CD8^+ T cell magnification and HBV-specific CD8^+ CTL mediated cytotoxicity were investigated in vitro using HLA-A2^+ human peripheral blood mononuclear cells (PBMCs) from healthy donors and chronic hepatitis B patients.RESULTS: Results demonstrated that the therapeutic polypeptides based on immunodominant HBcAg18-27 CTL,PreS2 B- and universal TN epitopes could stimulate the activation and proliferation of lymphocytes, induce specifically and effectively CD8+ T cell expansion and vigorous HBVspecific CTL-mediated cytotoxicity in human PBMCs.CONCLUSION: It indicated that the introduction of immunodominant T helper plus B-epitopes with short and flexible linkers could dramatically improve the immunogenicity of short CTL epitopes in vitro. | Tong-DongShi Yu-ZhangWu Zheng-CaiJia Li-YunZou WeiZhou | 2004 | World Journal of Gastroenterology2004，10，13： | 13 |
| 9 | 特利加压素联合大剂量白蛋白治疗肝硬化肝肾综合征的疗效观察显示文摘目的观察特利加压素及其联合大剂量白蛋白治疗肝肾综合征的疗效。方法53例患者分为三组,在综合治疗的基础上,A组使用多巴胺,B组使用特利加压素,C组使用特利加压素联合大剂量白蛋白,治疗期间观察患者临床症状、尿量、血肌酐、腹水消长情况,终止治疗事件及治疗后的转归。结果B、C组尿量、肌酐清除率显著增加,血肌酐降低,且C组变化比B组明显,A组仅轻度改善,三组间比较有显著差异。结论特利加压素对肝肾综合征的治疗有确切的疗效,大剂量白蛋白扩容可提高特利加压素对肾功能的作用。 | 孙亚冬 任祖海 叶启发 | 2007 | 实用肝脏病杂志2007，10，2： | 11 |
| 10 | 莪术油影响宫颈癌细胞MHC-Ⅰ类抗原呈递相关基因表达水平的实验研究显示文摘目的通过观察莪术油对体外培养宫颈癌细胞HeLa的增殖抑制及人类主要组织相容性复合物(major histocompatibility complex, MHC)Ⅰ类分子抗原呈递通路相关基因表达水平的影响,为莪术油应用于临床宫颈高危型人乳头瘤病毒(human papilloma virus,HPV)感染的治疗提供实验依据。方法以宫颈癌HeLa细胞为研究对象,体外培养HeLa细胞,绘制细胞生长曲线,CCK8法检测莪术油对细胞增殖抑制的作用,计算半数有效量(median effective dose,ED_(50));以不同剂量莪术油和干扰素干预细胞,收集不同作用时间的细胞样本,实时荧光定量PCR法检测样本中MHC-Ⅰ类抗原呈递通路相关基因人类白细胞抗原-Ⅰ(human leukocyte antigen, HLA-Ⅰ)、抗原处理相关转运蛋白1(transporter associated with antigen processing 1, TAP1)、抗原处理相关转运蛋白2(transporter associated with antigen processing 2, TAP2)的表达水平。结果各浓度莪术油混悬液对HeLa细胞有不同程度的抑制作用,高剂量莪术油(213.8μg/mL)可上调HeLa细胞HLA-Ⅰ、TAP1、TAP2的基因表达,且上调作用优于干扰素(P<0.05);干预12 h开始显效,其中HLA-Ⅰ基因表达在干预12 h达到最佳上调作用,之后上调作用减弱,TAP1、TAP2基因表达在干预48 h达到最佳上调作用(P<0.05)。结论莪术油可以上调宫颈癌HeLa细胞HLA-Ⅰ、TAP1、TAP2的基因表达,从而加强宫颈癌细胞表面的抗原呈递,避免病变细胞免疫逃逸,帮助机体清除HPV感染及癌变细胞,这可能是莪术油治疗宫颈HPV感染及宫颈癌的作用机制之一。另外,提示临床应用莪术油时,应使用高剂量并每日给药2次持续给药方能达到最佳治疗效果。 | 贾静 李云波 王群 | 2018 | 中国中西医结合杂志2018，38，11： | 8 |
| 11 | Expression of transforming growth factor-α and hepatitis B surface antigen in human hepatocellular carcinoma tissues and its significance显示文摘AIM:To evaluate the expression of transforming growthfactor-alpha (TGF-α) and hepatitis B surface antigen (HBsAg) in human hepatocellular carcinoma (HCC) tissues and its significance.METHODS:Seventy specimens of HCC tissues were detected by immunohistochemical method. Five specimens of normal human liver tissues were used as control.RESULTS: The TGF-o~ positive expression rates in HCC and its surrounding tissues were 74.3%(52/70) and 88.1%(52/59), respectively. TGF-α positive granules were mainly in the cytoplasm and fewer existed on the karyotheca. The TGF-α positive expressing rate in well differentiated HCC was significantly higher than that in moderately and poorly differentiated HCC (P<0.05).The TGF-α positive expression also was observed in intrahepatic bile ducts (part of those were hyperplastic ducts).The HBsAg positive expression rates in HCC and its surrounding tissues were 21.4%(15/70) and 79.7%(47/59), respectively.HBsAg positive granules were in the cytoplasm, inclusion and on the karyotheca.There was a prominent positive correlation between TGF-α and HBsAg expression in HCC surrounding tissues (P<0.05,γ=0.34). TGF-α was usually existed with HBsAg in regenerated and/or dysplastic liver cells.In the five normal liver tissues, TGF-α and HBsAg were not detectable in hepatocytes and bile ducts.CONCLUSION:Hepatitis B virus infection is dosely related with hepatocarcinogenesis.The overexpression of TGF-α in the liver seems to be associated with the regeneration of hepatocytes injured by HBsAg.The continued expression of TGF-α might lead to dysplasia of liver cells and development of HCC. Furthermore, TGF-α might play a role in morphogenesis and regeneration of intrahepatic bile ducts. | JingZhang Wen-LiangWang QingLi QingQiao | 2004 | World Journal of Gastroenterology2004，10，6： | 6 |
| 12 | 槲皮素联合顺铂对胃癌SGC-7901细胞增生和凋亡的影响显示文摘目的:探讨槲皮素(quercetin,QU)联合顺铂(DDP)对胃癌SGC-7901细胞增生、凋亡及凋亡相关基因Bcl-XL mRNA表达的影响. 方法:用槲皮素和顺铂处理胃癌SGC-7901细胞后,应用光镜、电镜、MTT法、流式细胞仪和RT-PCR 技术研究胃癌细胞的形态学变化、生长抑制、诱导凋亡和对凋亡相关基因Bcl-XL mRNA表达的影响. 结果:药物作用于细胞24 h后,可看到较为典型的细胞凋亡形态学变化.DDP和QU均可以抑制胃癌SGC-7901 细胞增生或诱导其凋亡,且有时间和剂量依赖效应,联合应用具有协同效应.联合组的诱导凋亡率及增生抑制效应显著高于单用DDP组(P<0.01),干预48 h后,Bcl- XLmRNA的表达下调,QU可以加强下调作用. 结论:人胃癌SGC-7901细胞体外实验中,QU和顺铂可以抑制其增生并诱导凋亡,二者联合应用有一定的协同效应,且呈剂量依赖关系. | 王海忠 王沁 | 2005 | 世界华人消化杂志2005，13，3： | 6 |
| 13 | 炎症性肠病的诊治进展显示文摘 | 姜敏 李红菊 | 2007 | 中国实用内科杂志2007，27，1： | 5 |
| 14 | 肝肾综合征的病理生理及其内科治疗原则显示文摘 | 高志钧 魏守礼 尤红煜 张玉敏 | 2006 | 临床荟萃2006，21，4： | 5 |
| 15 | 肝肾综合征发病机制及药物治疗进展显示文摘 | 韦志明 | 2008 | 华夏医学2008，21，4： | 4 |
| 16 | 大肠癌组织HLA-I类抗原及相关分子的表达意义显示文摘目的:探讨大肠癌组织HLA-Ⅰ类分子及相关分子表达及其意义. 方法:用免疫组化的方法,以切端黏膜作为正常对照,检测大肠癌组织、癌旁组织和正常黏膜组织中HLA-Ⅰ类分子及相关分子的表达,并结合肿瘤的临床病理资料综合分析. 结果:受检的大肠癌组织中重链HLA-A位点、B/C位点及轻链beta2微球蛋白(β2M)较其相应正常黏膜表达明显下调(P=0.0001);肠癌中低分子量多肽(LMP2)(P=0.0001),钙联蛋白(calnexin)(P=0.004)较正常黏膜表达明显下调;肠癌中HLA-Ⅰ类分子表达与肿瘤分化无关;随着肿瘤的Dukes 分期,癌组织中HLA-Ⅰ类分子表达渐次降低,但各位点表达情况并不相同,HLA-B/C表达水平与肿瘤分期相关,其在Dukes A期表达水平高于D期(P=0.0262). 结论:肠癌组织及癌旁黏膜中HLA-Ⅰ类分子、低分子量多肽及钙联蛋白较正常黏膜表达明显下调;肠癌组织中HLA- B/C位点随着肿瘤Dukes分期演进其表达下调. | 申龙树 黄培林 张建琼 | 2004 | 世界华人消化杂志2004，12，4： | 4 |
| 17 | 埃罗替尼和塞来昔布协同抑制胆管癌细胞生长显示文摘目的:观察表皮生长因子受体(EGFR)酪氨酸激酶抑制剂埃罗替尼(erlotinib)与环氧合酶(COX-2)抑制剂塞来昔布(celecoxib)对胆管癌细胞生长的协同抑制作用。方法:采用甲基噻唑基四唑(MTT)比色法检测胆管癌细胞株QBC939增殖,流式细胞术检测用药前、后细胞凋亡和细胞周期的变化,逆转录聚合酶链反应(RT-PCR)、Western印迹方法观察用药前、后细胞中COX-2、EGFR下游信号及凋亡、细胞周期相关基因蛋白表达的变化。结果:QBC939细胞表达COX-2 mRNA和EGFR mRNA及相应蛋白。埃罗替尼、塞来昔布抑制QBC939细胞增殖,促进细胞凋亡,诱导细胞周期阻滞于G0/G1期。同时,塞来昔布增强了埃罗替尼抑制细胞生长、诱导细胞凋亡的作用。联合用药显著降低p-MAPK、p-Akt及PGE2表达。结论:塞来昔布和埃罗替尼均可抑制胆管癌细胞的生长,而联合用药具有协同作用,能同时阻断EGFR和COX-2信号通路。在胆管癌治疗中具有一定应用前景。 | 李勤裕 施敏敏 杨卫平 彭承宏 | 2010 | 外科理论与实践2010，15，4： | 4 |
| 18 | 肝肾综合征的诊断及治疗进展显示文摘 | 王莉 袁孟彪 | 2004 | 临床肝胆病杂志2004，20，1： | 4 |
| 19 | 塞莱西布体外对人类肝胃癌细胞生长的抑制作用显示文摘目的:研究塞莱西布在体外对人类肝癌7721细胞以及胃癌7901细胞的生长抑制作用. 方法:两种肿瘤细胞用含不同浓度(0,20,40,80,160 和320 μmol/L)的塞莱西布的培养液培养.应用MTT测定法来测定生长抑制率,电镜技术来观察细胞凋亡情况,免疫组化技术来检测细胞内Cox-2蛋白含量. 结果:塞莱西布对两种肿瘤细胞均具有生长抑制作用(塞莱西布320μmol/L时两种肿瘤细胞抑制率分别为49.1%和42.9%), 并呈现量-效关系.电镜下可观察到凋亡细胞.免疫组化发现细胞内环氧化酶的含量在处理前后有明显变化. 结论:在体外,塞莱西布抑制人类肝癌及胃癌细胞生长, 诱导他们产生凋亡,并且该作用与细胞内环氧化酶含量有密切关系. | 樊菁 窦科峰 李开宗 | 2004 | 世界华人消化杂志2004，12，3： | 3 |
| 20 | 肝肾综合征的诊断与防治进展显示文摘 | 戴树人 高昆 易智慧 | 2006 | 中国误诊学杂志2006，6，1： | 3 |
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