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| 1 | C/S到B/S模式转换的技术研究显示文摘随着Internet技术的兴起,致使更多的企业着手将C/S模式向B/S模式迁移。针对传统软件复用技术,对现有C/S模式的遗留系统进行分析,提出一种由C/S模式到B/S模式转换的方法。采用虚拟应用技术和.NET框架下的UIA技术,使用XML文件作为信息交换的载体,实现浏览器对C/S软件的远程操作,利用现有资源完成B/S结构的开发,并且无需修改源C/S软件的代码,体现模式的平台无关性,具有界面统一性、高度可扩展性以及易维护性等特征。实验结果表明,该方法在Windows XP的计算器中得到成功应用。 | 查修齐 吴荣泉 高元钧 | 2014 | 计算机工程2014，40，1： | 70 |
| 2 | Immune suppression in chronic hepatitis B infection associated liver disease: A review显示文摘Hepatitis B virus(HBV) infection is one the leading risk factors for chronic hepatitis, liver fibrosis, cirrhosis and hepatocellular cancer(HCC), which are a major global health problem. A large number of clinical studies have shown that chronic HBV persistent infection causes the dysfunction of innate and adaptive immune response involving monocytes/macrophages, dendritic cells, natural killer(NK) cells, T cells. Among these immune cells, cell subsets with suppressive features have been recognized such as myeloid derived suppressive cells(MDSC),NK-reg, T-reg, which represent a critical regulatory system during liver fibrogenesis or tumourigenesis. However, the mechanisms that link HBVinduced immune dysfunction and HBV-related liver diseases are not understood.In this review we summarize the recent studies on innate and adaptive immune cell dysfunction in chronic HBV infection, liver fibrosis, cirrhosis, and HCC, and further discuss the potential mechanism of HBV-induced immunosuppressive cascade in HBV infection and consequences. It is hoped that this article will help ongoing research about the pathogenesis of HBV-related hepatic fibrosis and HBV-related HCC. | Tian-Yang Li Yang Yang Guo Zhou Zheng-Kun Tu | 2019 | World Journal of Gastroenterology2019，25，27： | 69 |
| 3 | Animal experiment and clinical study of effect of gamma-interferon on hepatic fibrosis显示文摘AIM To evaluate the antifibrotic effect ofdifferent doses of recombinant human Gamma-Interferon (IFN-γ) intwo rat models of hepaticfibrosis, and to observe its effect on moderatechronic hepatitis B virus fibrosis.METNODS Hepatic fibrosis was successfullyinduced in 150 and 196 rats by subcutaneousinjection of carbon tetrachloride (CCl4) andintraperitoneal injection of dimethylnitrosamine(DMN), respectively. Each of the two modeldose IFN-γ group (15 MU/kg per day, i.m. for 8group (1.67 MU/kg daily, i.m. for 8 weeks).Another group of 10 rats without any treatmentwas used as normal controls. At the end of theexperiment, semi-quantitative histopathologicalscores of inflammation and fibrosis, liver (αsmooth muscle actin (α-SMA) expression level,liver hydroxyl proline content and serumhyaluronic acid levels were compared. And 47medium chronic hepatitis B viral fibrosispatients were studied. They were given IFN-γtreatment, 100MU/day i.m. for the first threemonths and 100MU qod i.m. for the next sixmonths. Semi-quantitative pathological scoresof inflammation and fibrosis and serum hepaticfibrosis indices were compared within the 9months.RESULTS In animal experiment, thepathological fibrosis scores and liver hydroxylproline content were found to be significantlylower in rats treated with different doses of IFN-γ as compared with rats in fibrotic model groupinduced by either CCI4 or DMN, in a dose-dependent manner. For CCI4-induced model,pathological fibrosis scores in high, medium andIow doses IFN-γ groups were 5.10 ± 2.88, 7.70 ±3.53 and 8.00 ± 3.30, respectively, but the scorewas 14.60 ± 7.82 in fibrotic model group.Hydroxyl proline contents were 2.83 ± 1.18, 3.59± 1.22 and 4.80 ± 1.62, in the three IFN-γgroups, and 10.01 ± 3.23 in fibrotic model group.The difference was statistically significant(P<0.01). Similar results were found in DMN-induced model. Pathological fibrosis scoreswere 6.30±0.48, 8.10 ±2.72 and 8.30 ±2.58, inhigh, medium and Iow doses IFN-γ groups, and12.60 ± 3.57 in fibrotic model group. Hydroxylproline contents were 2.72 ± 0.58, 3.14 ± 0.71and 3.62 ± 1.02, in the three IFN-γ groups, and12.79 ± 1.54 in fibrotic model group. Thedifference was statistically significant(P<0.01). Serum hepatic fibrosis indicesdecreased significantly in the 47 patients afterIFN-γ treatment (HA: 433.38 ± 373.00 vs 281.57± 220.48; LN: 161.22± 41.02 vs 146.35 ± 44.67;PCⅢ: 192.59 ± 89.95 vs 156.98 ± 49.22; C-Ⅳ:156.30 ± 44.01 vs 139.14 ± 34.47) and thedifferences between the four indices weresignificant (P<0.05). Thirty-three patientsCONCLUSION All the three doses of IFN-γ areeffective in treating rat liver fibrosis induced byeither CCl4 or DMN, the higher the dose, thebetter the effect. And IFN-γ is effective forpatients with moderate chronic hepatitis B viralfibrosis. | Hong Lei Weng Wei Min Cai Rong Hua Liu Institute of Infectious Diseases, First Affiliated Hospital. Medical School. Zhejiang University, Hangzhou 310003, Zhejiang Province. China | 2001 | World Journal of Gastroenterology2001，7，1： | 53 |
| 4 | 可见光/Fenton光催化降解有机染料显示文摘采用Fenton试剂(Fe3+/H2O2)在可见光条件下(λ>450 nm)光催化降解目标染料化合物罗丹明B(Rhodam ine B,RhB).在pH<3.0体系中用可见光照射,能使RhB染料在光敏化作用下有效降解,反应160m in后矿化率达到71.8%.采用ESR和溴甲酚绿(B romocresol green,BCG)法跟踪测定活性氧化物种,通过对RhB降解过程的紫外-可见光谱、红外光谱分析及总有机碳量(TOC)跟踪测定,结果表明,Fe3+/H2O2/RhB体系在可见光照射下主要的活性氧化物种为羟基自由基,能有效地降解RhB. | 黄应平 刘德富 张水英 张德莉 马万红 赵进才 | 2005 | 高等学校化学学报2005，26，12： | 56 |
| 5 | 长江河口区第四纪沉积物中的地球化学元素分布特征及其古环境意义显示文摘文章通过对上海浦东机场孔(Pd)第四纪地层中地球化学微量元素B,Ga,Sr和Ba的观测,结合该钻孔粒度、古地磁和微体古生物等分析资料,综合剖析了这些微量元素及其比值在不同沉积相中的分布特征及其古环境演变的意义.研究发现,微量元素分布与本区各种沉积相有着十分密切的关系.通常,B和Sr及其比值B/Ga和Sr/Ba在冲积相、河流相沉积中较低,在溺谷-浅海相、三角洲相沉积中较高.而Ba与之相反,一般在陆相沉积环境中比较高.Ga元素在第四纪沉积物中的分布波动不明显,但极大值还是偏向陆相环境.本研究还发现微量元素B和Sr及其比值B/Ga,Sr/Ba的分布自下而上存在7个(1~7)高值阶段.阶段1~3高值与海侵无关,认为反映了上新世-早更新世干旱气候的产物;阶段4~7高值则与本区中更新世以来4次海侵事件密切相关. | 韦桃源 陈中原 魏子新 王张峤 王张华 殷鸿福 | 2006 | 第四纪研究2006，26，3： | 52 |
| 6 | Detection of serum TNF-α,IFN-γ,IL-6 and IL-8 in patients with hepatitis B显示文摘NTRODUCTIONSinceMuto[1]reportedthatTNFαandIL1wererelatedtofulminanthepatitis,thestudiesontherelationshipbetweencytokinesa... | WANG Jing Yan, WANG Xue Lian and LIU Pei | 1999 | World Journal of Gastroenterology1999，5，1： | 54 |
| 7 | NF-κB的信号通路与阻断策略显示文摘NF-κB is thought of as a genetic switch to control expressions of many target genes and directly participates in pathogenesis of infection, inflammation, stress, immunoresponse, cellular apoptosis, toxic shock and tumor as well as cell-cycle regulation and cell differentiation. The overactivation of NF-κB is intimately involved in many human diseases. Various therapeutic strategies against NF-κB, to date, include anti-inflammatory drugs, antioxidants, immunosuppressive agents, inhibitors of protease and proteasome, prostaglandings, nitric oxide, IL-10, microbial products, synthetic inhibitors, antisense oligonucleotides and decoy deoxyoligonucleotides. Studies are underway to develop NF-κB member-specific and cell type-specific drugs that can inhibit the activation of NF-κB only in target cells and that may become a novel way to treat the human diseases. | 邢飞跃 赵克森 姜勇 | 2003 | 中国病理生理杂志2003，19，6： | 53 |
| 8 | Gut-liver axis and probiotics: Their role in non-alcoholic fatty liver disease显示文摘The incidence of obesity and its related conditions, including non-alcoholic fatty liver disease(NAFLD), has dramatically increased in all age groups worldwide. Given the health consequences of these conditions, and the subsequent economic burden on healthcare systems, their prevention and treatment have become major priorities. Because standard dietary and lifestyle changes and pathogenically-oriented therapies(e.g., antioxidants, oral hypoglycemic agents, and lipid-lowering agents) often fail due to poor compliance and/or lack of efficacy, novel approaches directed toward other pathomechanisms are needed. Here we present several lines of evidence indicating that, by increasing energy extraction in some dysbiosis conditions or small intestinal bacterial overgrowth,specific gut microbiota and/or a'low bacterial richness'may play a role in obesity,metabolic syndrome,and fatty liver.Under conditions involving a damaged intestinal barrier('leaky gut'),the gut-liver axis may enhance the natural interactions between intestinal bacteria/bacterial products and hepatic receptors(e.g.,toll-like receptors),thus promoting the following cascade of events:oxidative stress,insulinresistance,hepatic inflammation,and fibrosis.We also discuss the possible modulation of gut microbiota by probiotics,as attempted in NAFLD animal model studies and in several pilot pediatric and adult human studies.Globally,this approach appears to be a promising and innovative add-on therapeutic tool for NAFLD in the context of multi-target therapy. | Giulia Paolella Claudia Mandato Luca Pierri Marco Poeta Martina Di Stasi Pietro Vajro | 2014 | World Journal of Gastroenterology2014，20，42： | 55 |
| 9 | Diagnostic value of PIVKA-Ⅱ and alpha-fetoprotein in hepatitis B virus-associated hepatocellular carcinoma显示文摘AIM: To determine the cutoff values and to compare the diagnostic role of alpha-fetoprotein(AFP) and prothrombin induced by vitamin K absence-Ⅱ(PIVKA-Ⅱ) in chronic hepatitis B(CHB).METHODS: A total of 1255 patients with CHB, including 157 patients with hepatocellular carcinoma(HCC), 879 with non-cirrhotic CHB and 219 with cirrhosis without HCC, were retrospectively enrolled. The areas under the receiver operating characteristic(AUROC) curves of PIVKA-Ⅱ, AFP and their combination were calculated and compared.RESULTS: The optimal cutoff values for PIVKA-Ⅱ and AFP were 40 m AU/m L and 10 ng/m L, respectively, for the differentiation of HCC from nonmalignant CHB. The sensitivity and specificity were 73.9% and 89.7%, respectively, for PIVKA-Ⅱ and 67.5% and 90.3% for AFP, respectively. The AUROC curves of both PIVKA-Ⅱ and AFP were not significantly different(0.854 vs 0.853, P = 0.965) for the differentiation of HCC from nonmalignant CHB, whereas the AUROC of PIVKA-Ⅱ was significantly better than that of AFP in patients with cirrhosis(0.870 vs 0.812, P = 0.042). When PIVKA-Ⅱ and AFP were combined, the diagnostic power improved significantly compared to either AFP or PIVKA-Ⅱ alone for the differentiation of HCC from nonmalignant CHB(P < 0.05), especially when cirrhosis was present(P < 0.05).CONCLUSION: Serum PIVKA-Ⅱ might be a better tumor marker than AFP, and its combination with AFP may enhance the early detection of HCC in patients with CHB. | Seung In Seo Hyoung Su Kim Won Jin Kim Woon Geon Shin Doo Jin Kim Kyung Ho Kim Myoung Kuk Jang Jin Heon Lee Joo Seop Kim Hak Yang Kim Dong Joon Kim Myung Seok Lee Choong Kee Park | 2015 | World Journal of Gastroenterology2015，21，13： | 60 |
| 10 | A randomized controlled clinical trial on the treatment of Thymosin-a1 versus interferon-α in patients with hepatitis B显示文摘INTRODUCTIONChronic hepatitis B virus (HBV) infection is a serious problem because of its world wide distribution and possible adverse sequelae ,such as cirrhosis and hepatocellular carcinoma .The World Health Organization estimates that HBV has infected mord than 350 million people worldwide ,and up to 20% of them will become chromic carricrs and will be at significant risk for cirrhosis and HCC .The ultimate goal of the therapy for chronic hepatitis B is to prevent progression to cirrhosis and to prevent development of HCC. | Jing You Lin Zhuang Bao Zhang Tang Wei Bo Yang Su Ying Ding Wu Li Rong Xue Wu Hong Li Zhang Yan Mei Zhang Shao Ming Yan Lu Zhang ~1Department of Infectious Diseases,The First Affiliated Hospital of Kunming Medical College,Kunming 650032,Yunnan Province,China ~2Departrnent of Hepatology,Kunming Third Municipal People’s Hospital,Kunming 650041,Yunnan Province,China | 2001 | World Journal of Gastroenterology2001，7，3： | 48 |
| 11 | 紫外线的皮肤损伤机制及具有紫外线防护作用的天然产物的研究进展显示文摘皮肤长期暴露在紫外线下可以引起皮肤损伤,出现皮肤光老化甚至出现皮肤癌变和其他皮肤病变。紫外线引起的皮肤光老化的主要机制有:氧化应激、炎症反应、细胞凋亡、胶原和弹性蛋白的降解等。目前国内外关注的焦点是开发紫外线防护剂,目前主要研究的有黄酮类化合物、萜类化合物、鞣质类、香豆素类等。该文主要对紫外线的皮肤损伤机制及天然来源紫外线防护剂的研究进展进行综述。 | 路婷婷 陈亚泽 卢涛 张予阳 | 2012 | 中国药理学通报2012，28，12： | 43 |
| 12 | Th1/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC), the predominant type of primary liver cancer, is one of the most serious lifethreatening malignancies, worldwide. In majority of the cases, HCC develops after prolonged and persistent chronic liver disease. hepatitis B virus(HBV) or HCV infection is prominent etiological factors, attributing to this condition. It has been well documented that HBV, being the inducer of chronic inflammation, is the main causative agent in causing HCC, particularly in Asian countries. The HBV infection leads to a wide range of clinical symptoms from carrier state to malignancy. Cytokines being immune-modulatory molecules, are the key mediators in the defense mechanism against viral infection. In this regard, this review will detail the substantial role of key Th1: interleukin 1(IL-1), IL-2, IL-12, tumor necrosis factor-α, interferon-γ; Th2: IL-4, IL-10 and non Th1/Th2: IL-6, transforming growth factor-β1 cytokines genotypes in analyzing the variability in the clinical manifestations in an HBV-afflicted individual, which might finally, culminates into HCC. Since cytokine production is regulated genetically, the cytokine promoter region single-nucleotide polymorphisms induced changes, greatly affects the cytokine production, thus resulting into differential outcome of immune balance. | Roli Saxena Jyotdeep Kaur | 2015 | World Journal of Hepatology2015，7，11： | 50 |
| 13 | 香砂六君子汤对菌致慢性萎缩性胃炎TLR信号通路的影响显示文摘为研究香砂六君子汤对幽门螺杆菌相关性胃炎(HAG)大鼠的疗效及其对Toll样受体(Toll likereceptors,TLR)信号通路的影响。将60只清洁级的SD大鼠随机分为6组:正常对照组,模型组,香砂六君子汤组(低、中、高剂量3组)以及抑制剂(SB203580)组。通过采用幽门螺杆菌(HP)灌胃构建慢性萎缩性胃炎模型。组织病理检测胃黏膜组织的病变情况;ELISA检测TNF-α,IL-6含量以及iNOS的活性;硝酸还原酶法测定NO的含量;QPCR,Western-blot检测胃黏膜组织TLR2,TLR4,P38MAPK,NF-κB基因的表达情况。结果显示,大鼠模型组与正常对照组相比,胃黏膜组织TLR2,TLR4,p-P38MAPK蛋白以及细胞核内NF-κB蛋白表达均增加(P<0.01);与模型组相比,香砂六君子汤组大鼠胃黏膜TLR2,TLR4,p-P38MAPK蛋白以及细胞核内NF-κB蛋白表达逐渐降低,以高剂量组降低最为明显(P<0.01),且HP根除率逐渐提高、慢性萎缩性胃炎的病理变化逐渐减轻。结果表明,在大鼠模型中,HP通过激活TLR2,TLR4/MAPK/NF-κB/iNOS/NO信号通路诱发慢性萎缩性胃炎的病理改变,香砂六君子汤能根除HP,可减轻HP引起的慢性萎缩性胃炎的黏膜炎症反应。该中药方剂治疗HP所致的慢性萎缩性胃炎既安全又有效。 | 林志强 王大璇 洪珊珊 傅新阳 | 2016 | 中国中药杂志2016，41，16： | 47 |
| 14 | Entecavir vs lamivudine therapy for na?ve patients with spontaneous reactivation of hepatitis B presenting as acute-on-chronic liver failure显示文摘AIM:To investigate the short-term and long-term efficacy of entecavir versus lamivudine in patients with spontaneous reactivation of hepatitis B presenting as acute-on-chronic liver failure(ACLF).METHODS:This was a single center,prospective cohort study.Eligible,consecutive hospitalized patients received either entecavir 0.5 mg/d or lamivudine 100mg/d.All patients were given standard comprehensive internal medicine.The primary endpoint was survival rate at day 60,and secondary endpoints were reduction in hepatitis B virus(HBV)DNA and alanine aminotransferase(ALT)levels,and improvement in Child-Turcotte-Pugh(CTP)and model for end-stage liver disease(MELD)scores at day 60 and survival rate at week 52.RESULTS:One hundred and nineteen eligible subjects were recruited from 176 patients with severe acute exacerbation of chronic hepatitis B:65 were included in the entecavir group and 54 in the lamivudine group(full analysis set).No significant differences were found in patient baseline clinical parameters.At day 60,entecavir did not improve the probability of survival(P=0.066),despite resulting in faster virological suppression(P<0.001),higher rates of virological response(P<0.05)and greater reductions in the CTP and MELD scores(all P<0.05)than lamivudine.Intriguingly,at week 52,the probability of survival was higher in the entecavir group than in the lamivudine group[42/65(64.6%)vs 26/54(48.1%),respectively;P=0.038].The pretreatment MELD score(B,1.357;95%Cl:2.138-7.062;P=0.000)and virological response at day30(B,1.556;95%Cl:1.811-12.411;P=0.002),were found to be good predictors for 52-wk survival.CONCLUSION:Entecavir significantly reduced HBV DNA levels,decreased the CTP and MELD scores,and thereby improved the long-term survival rate in patients with spontaneous reactivation of hepatitis B presenting as ACLF. | Yang Zhang Xiao-Yu Hu Sen Zhong Fang Yang Tao-You Zhou Guo Chen Yan-Yan Wang Jian-Xing Luo | 2014 | World Journal of Gastroenterology2014，20，16： | 42 |
| 15 | Hepatitis B virus genotypes:Global distribution and clinical importance显示文摘At least 600000 individuals worldwide annually die of hepatitis B virus(HBV)-related diseases,such as chronic hepatitis B(CHB),liver cirrhosis(LC),and hepatocellular carcinoma(HCC).Many viral factors,such as viral load,genotype,and specific viral mutations,are known to affect disease progression.HBV reverse transcriptase does not have a proofreading function,therefore,many HBV genotypes,sub-genotypes,mutants,and recombinants emerge.Differences between genotypes in response to antiviral treatment have been determined.To date,10 HBV genotypes,scattered across different geographical regions,have been identified.For example,genotype A has a tendency for chronicity,whereas viral mutations are frequently encountered in genotype C.Both chronicity and mutation frequency are common in genotype D.LC and progression to HCC are more commonly encountered with genotypes C and D than the other genotypes.Pathogenic differences between HBV genotypes explain disease intensity,progression to LC,and HCC.In conclusion,genotype determination in CHB infection is important in estimating disease progression and planning optimal antiviral treatment. | Mustafa Sunbul | 2014 | World Journal of Gastroenterology2014，20，18： | 42 |
| 16 | Management of chronic hepatitis B infection: Current treatment guidelines, challenges, and new developments显示文摘Chronic hepatitis B(CHB)virus infection is a global public health problem,affecting more than 400 million people worldwide.The clinical spectrum is wide,ranging from a subclinical inactive carrier state,to progressive chronic hepatitis,cirrhosis,decompensation,and hepatocellular carcinoma.However,complications of hepatitis B virus(HBV)-related chronic liver disease may be reduced by viral suppression.Current international guidelines recommend first-line treatment of CHB infection with pegylated interferon,entecavir,or tenofovir,but the optimal treatment for an individualpatient is controversial.The indications for treatment are contentious,and increasing evidence suggests that HBV genotyping,as well as serial on-treatment measurements of hepatitis B surface antigen and HBV DNA kinetics should be used to predict antiviral treatment response.The likelihood of achieving a sustained virological response is also increased by extending treatment duration,and using combination therapy.Hence the paradigm for treatment of CHB is constantly evolving.This article summarizes the different indications for treatment,and systematically reviews the evidence for the efficacy of various antiviral agents.It further discusses the shortcomings of current guidelines,use of rescue therapy in drug-resistant strains of HBV,and highlights the promising clinical trials for emerging therapies in the pipeline.This concise overview presents an updated practical approach to guide the clinical management of CHB. | Ceen-Ming Tang Tung On Yau Jun Yu | 2014 | World Journal of Gastroenterology2014，20，20： | 41 |
| 17 | Changes in circulating Foxp3^+ regulatory T cells and interleukin-17-producing T helper cells during HBV-related acute-on-chronic liver failure显示文摘AIM:To longitudinally investigate cytokine gene expression and protein levels in Th17 and Treg cells,to observe T-cell phenotypes during hepatitis B virus(HBV)-related acute-on-chronic liver failure(ACHBLF)and to analyze changes in Th17 and Treg phenotypes during disease progression.METHODS:We measured the expression of seven Th17/Treg differentiation-related genes and serum concentrations of the corresponding cytokines in 18ACHBLF,18 chronic hepatitis B(CHB)disease controls and 10 healthy controls(HCs)by real-time quantitative pCR and enzyme linked immunosorbent assay.peripheral Th17 and Treg cell frequencies were analyzed by flow cytometry.RESULTS:From the onset of ACHBLF,patients presented with a conductive Th17 differentiation cytokine environment accompanied by high Th17 frequency and high serum IL-17 levels,which were sustained throughout the disease course.The Treg-related cytokine IL-2and Foxp3 were also up-regulated from disease onset,and Foxp3 gene expression showed a gradually increasing trend during ACHBLF.The circular phenotype of Treg and Th17 cells showed changes from the onset of ACHGLF.At disease onset,Th17 frequency increased significantly compared with both CHB and HCs,but Treg cell frequency decreased significantly compared with CHB.During the ACHBLF event,Th17 frequency remained higher compared with HCs,but decreased sharply from the peak point to the recovery point;Treg cell frequency increased gradually during the ACHBLF event.Treg and Th17 cell counts correlated with ACHBLF development;in all patients,serum IL-17 levels significantly correlated with patient serum ALT levels.In survivors,Th17 frequency at the onset point and the Treg to Th17 ratio at the peak point correlated with the patient’s model for end stage liver disease(MELD)plus sodium(MELD-Na)score.The Treg to Th17 ratio and the Th17 frequency at onset were significant predictors of patient survival.Low Treg/Th17 cell ratios at the onset predicted poor survival.Survivors exhibited an initial decrease in the circulating Treg/Th17 ratio from the onset to the peak time,and subsequently displayed a continuous increase.CONCLUSION:Treg and Th17 cells showed changes in genes,protein levels and T cell phenotypes during ACHBLF events.An increased Treg/Th17 ratio was associated with the survival of ACHBLF patients. | Xue-Song Liang Cheng-Zhong Li Yin Zhou Wei Yin Ya Yun Liu Wen-Han Fan | 2014 | World Journal of Gastroenterology2014，20，26： | 44 |
| 18 | Hepatitis B:Epidemiology and prevention in developing countries显示文摘Hepatitis B virus(HBV)infection is a serious global public health problem.The infection may be transmitted through sexual intercourse,parenteral contact or from an infected mother to the baby at birth and,if contracted early in life,may lead to chronic liver disease,including cirrhosis and hepatocellular carcinoma.On the basis of the HBV carrier rate,the world can be divided in 3 regions of high,medium and low endemicity.The major concern is about high endemicity countries,where the most common route of infection remains vertical transmission from mother to child.Screening of all pregnant women and passive immunization with human hepatitis B immunoglobulin are not affordable for many developing countries.The infection rate can be reduced by modifying behavior,improving individual education,testing all blood donations,assuring asepsis in clinical practice and screening all pregnant women.However,availability of a safe and efficacious vaccine and adoption of appropriate immunization strategies are the most effective means to prevent HBV infection and its consequences.The unsolved problem for poorest countries,where the number of people currently infected is high,is the cost of the vaccine.A future challenge is to overcome the social and economic hurdles of maintaining and improving a prevention policy worldwide to reduce the global burden of the disease. | Elisabetta Franco Barbara Bagnato Maria Giulia Marino Cristina Meleleo Laura Serino Laura Zaratti | 2012 | World Journal of Hepatology2012，4，3： | 39 |
| 19 | Antiviral therapy for hepatitis B virus associated hepatic failure显示文摘BACKGROUND:Chronic hepatitis B virus(HBV)infection remains a major global health issue,and the prognosis of patients with HBV-associated fulminant hepatic failure is extremely poor.The application of antiviral therapies has led to significant improvements in patient outcomes.This article aimed to review the current strategies in antiviral treatment of HBV-associated fulminant hepatic failure. DATA SOURCES:Literature search was conducted using PubMed on the related subjects.Part of the data was from the most recent work of the authors’laboratory. RESULTS:Hepatitis B immunoglobulin in prevention of recurrent HBV infection after orthotopic liver transplantation(OLT)has been proven effective.However, its cost is high,and significant side effects have been found to induce viral mutations.Lamivudine has a potent suppression for HBV replication and an excellent safety profile in decompensated cirrhotic patients,but its major drawback is the high rate of drug-resistance.Adefovir is effective for lamivudine-resistance strains in the post- OLT situation,and its drug-resistance rate is relatively low. Combination therapies such as hepatitis B immunoglobulin combined with lamivudine and lamivudine combined with adefovir have been widely adopted for prophylaxis against HBV recurrence of infection after OLT.Entecavir, telbivudine,tenofovir and other newer agents have been widely used in antiviral therapy. CONCLUSIONS:The prognosis of HBV-associated ful- minant hepatic failure is being transformed by developments in antiviral therapy.However,it should be noticed that HBV is controlled but never eliminated,and drug-resistance still remains a major issue.Hopefully,newer strategies may help to solve these problems. | Wang, Yu-Ming Tang, Ying-Zi | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，1： | 36 |
| 20 | Expression of CXC chemokine IP-10 in patients with chronic hepatitis B显示文摘BACKGROUND: Chemokines have strong chemoattractant effects and are involved in a variety of immune and inflammatory reactions, such as attracting activated T lymphocytes, neutrophils, monocytes and natural killer cells via the pathway of G protein-coupled receptors to sites of inflammatory injury and contribute to wound repair. This investigation was designed to assess the levels of chemokine interferon-γ inducible protein-10 (IP-10) and IP-10 mRNA, and the relationship between IP-10 mRNA and HBV-DNA and alanine aminotransferase (ALT) in patients with chronic hepatitis B. METHODS: The levels of IP-10 mRNA in peripheral blood mononuclear cells (PBMCs) were kinetically detected by real-time polymerase chain reaction (PCR). The rate of chemokine/GAPDH was regarded as the extreme level of chemokine. The level of IP-10 in serum was measured by enzyme linked immunosorbent assay (ELISA), and the expression of IP-10 in hepatic biopsy tissue was detected by streptavidin-peroxidase (SP) immunohistochemistry. RESULTS: The level of IP-10 mRNA in the PBMCs of patients was 0.7387±0.0768 (lg cDNA/lg GAPDH); it was significantly higher in patients with chronic hepatitis B than that in normal controls (P<0.001). The level of IP-10 in the serum of patients was 660.9±75.5 pg/ml. There was a significant difference between patients with chronic hepatitis B and normal controls (P<0.05). In patients with chronic hepatitis B, the level of IP-10 mRNA in PBMCs was correlated with the IP-10 plasma level(r=0.7312, P<0.001), and the IP-10 plasma level was fairly correlated with the levels of ALT and HBV-DNA plasma (r=0.7235, P<0.001; r=0.7371, P<0.001). IP-10 was found by immunohistochemical analysis to be selectively upregulated on sinusoidal endothelium. CONCLUSIONS: The expression of IP-10 mRNA in PBMCs, IP-10 plasma concentration and the expression of IP-10 in sinusoidal endothelium are all high in patients with chronic hepatitis B. Chemokine IP-10 may play an important role in trafficking inflammatory cells to the local focus in the liver and induce the development of the chronicity of hepatitis B. | Wang, Jian Zhao, Jin-Hong Wang, Ping-Ping Xiang, Gui-Ju | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，1： | 36 |
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