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| 1 | 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 |
| 2 | HCV-RNA positivity in peripheral blood mononuclear cells of patients with chronic HCV-infection: does it really mean viral replication?显示文摘AIM To analyze the association of HCV-RNA with peripheral blood mononuclear cells (PBMC)and to answer the question whether HCV-RNA positivity in PBMC is due to viral replication,METHODS HCV-RNA was monitored in serumand PBMC preparations from 15 patients with chronic HCV infection before, during and after an IFN-α therapy using a nested RT/ PCRtechnique. In a second approach, PBMC from healthy donors were incubated in HCV positive plasma.RESULTS In the IFN-α responding patients,HCV-RNA disappeared first from total RNApreparations of PBMC and then from serum. In contrast, in relapsing patients, HCV-RNAreappeared first in serum and then in PBMC. A quantitative analysis of the HCV-RNAconcentration in serum was performed before and after transition from detectable to nondetectable HCV-RNA in PBMC-RNA and vice versa. When HCV-RNA was detectable in PBMCpreparations, the HCV concentration in serum was significantly higher than the serum HCV-RNA concentration when HCV-RNA in PBMC was not detectable. Furthermore, at no time during the observation period was HCV specific RNA observed in PBMC, if HCV-RNA in serum was under the detection limit. Incubation of PBMCfrom healthy donors with several dilutions of HCV positive plasma for two hours showed a concentration-dependent PCR-positivity for HCV-RNA in reisolated PBMC.CONCLUSION The detectability of HCV-RNA in total RNA from PBMC seems to depend on the HCV concentration in serum. Contamination or passive adsorption by circulating virus could be the reason for detection of HCV-RNA in PBMCpreparations of chronically infected patients. | Volker Meier Sabine Mihm Perdita Wietzke-Braun Guliano Ramadori | 2001 | World Journal of Gastroenterology2001，7，2： | 29 |
| 3 | Management of patients with hepatitis C infection and renal disease显示文摘Hepatitis C virus(HCV) infection in patients with end-stage renal disease(ESRD) is associated with more rapid liver disease progression and reduced renal graft and patients' survival following kidney transplantation. Evaluations and management of HCV in patients with renal disease are challenging. The pharmacokinetics of interferons(IFN), ribavirin(RBV) and some direct acting antiviral(DAA), such as sofosbuvir, are altered in patients with ESRD. With dose adjustment and careful monitoring, treatment of HCV in patients with ESRD can be associated with sustained virological response(SVR) rates nearly comparable to that of patients with normal renal function. DAA-based regimens, especially the IFNfree and RBV-free regimens, are theoretically preferred for patients with ESRD and KT in order to increase SVR rates and to reduce treatment side effects. However, based on the data for pharmacokinetics, dosing safety and efficacy of DAA for patients with severe renal impairment are lacking. This review will be focused on the evaluations, available pharmacologic data, and management of HCV in patients with severe renal impairment, patients who underwent KT, and those who suffered from HCV-related renal disease, according to the available treatment options, including DAA. | Chalermrat Bunchorntavakul Monthira Maneerattanaporn Disaya Chavalitdhamrong | 2015 | World Journal of Hepatology2015，7，2： | 25 |
| 4 | Plasmacytoid dendritic cells in antiviral immunity and autoimmunity显示文摘Plasmacytoid dendritic cells (pDCs) represent a unique and crucial immune cell population capable of producing large amounts of type I interferons (IFNs) in response to viral infection.The function of pDCs as the professional type I IFN-producing cells is linked to their selective expression of Toll-like receptor 7 (TLR7) and TLR9,which sense viral nucleic acids within the endosomal compartments.Type I IFNs produced by pDCs not only directly inhibit viral replication but also play an essential role in linking the innate and adaptive immune system.The aberrant activation of pDCs by self nucleic acids through TLR signaling and the ongoing production of type I IFNs do occur in some autoimmune diseases.Therefore,pDC may serve as an attractive target for therapeutic manipulations of the immune system to treat viral infectious diseases and autoimmune diseases. | TANG Fei1,2,DU Qiumei1,2 & LIU Yong-Jun3 1 Center for Infection and Immunity,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China 2 Graduate University of Chinese Academy of Sciences,Beijing 100049,China 3 Department of Immunology and Center for Cancer Immunology Research,University of Texas,M.D.Anderson Cancer Center,Houston,Texas 77030,USA | 2010 | Science China(Life Sciences)2010，53，2： | 23 |
| 5 | Effects of antiviral therapy on preventing liver tumorigenesis and hepatocellular carcinoma recurrence显示文摘Chronic hepatitis B virus(HBV)infection is the key driving force of liver disease progression,resulting in the development of hepatic dysfunction,cirrhosis and hepatocellular carcinoma(HCC).The primary aim of therapy is to suppress or eliminate HBV replication to reduce the activity of hepatitis,thus reducing the risk of,or slowing the progression of,liver disease.Nucleos(t)ide analogues(Nucs)may result in rapid suppression of HBV replication with normalization of serum transaminases and restore liver function,thus increasing survival in patients with hepatic decompensation.Long-term Nuc therapy may result in histological improvement or reversal of advanced fibrosis and reduction in disease progression,including the development of HCC.The long-term benefits of a finite course of interferon(IFN)-αtherapy also include a sustained and cumulative response,as well as hepatitis B surface antigen seroclearance and reduction in the development of cirrhosis and/or HCC.Pegylated IFN and newer Nucs may achieve better long-term outcomes because of improved efficacy and a low risk of drug resistance.However,treatment outcomes are still far from satisfactory.Understanding the effects of anti-HBV treatment against HCC incidence and recurrence after hepatectomy or liver transplantation is required for further improvement of outcome. | Zhong-Ming Tan Bei-Cheng Sun | 2013 | World Journal of Gastroenterology2013，19，47： | 22 |
| 6 | Antiviral treatment to prevent chronic hepatitis B or C-related hepatocellular carcinoma显示文摘Antiviral treatment is the only option to prevent or defer the occurrence of hepatocellular carcinoma(HCC) in patients chronically infected with hepatitis B virus(HBV) or hepatitis C virus(HCV). The approved medication for the treatment of chronic HBV infection is interferon-α(IFNα) and nucleos(t)ide analogues(NAs), including lamivudine, adefovir dipivoxil, telbivudine, entecavir and tenofovir disoproxil fumarate. IFNα is the most suitable for young patients with less advanced liver diseases and those infected with HBV genotype A. IFNα treatment significantly decreases the overall incidence of HBV-related HCC in sustained responders. However, side effects may limit its long-term clinical application. Orally administered NAs are typically implemented for patients with more advanced liver diseases. NA treatment significantly reduces disease progression of cirrhosis and therefore HCC incidence, especially in HBV e antigen-positive patients. NA-resistance due to the mutations in HBV polymerase is a major limiting factor. Of the NA resistance-associated mutants, A181 T mutant significantly increases the risk of HCC development during the subsequent course of NA therapy. It is important to initiate treatment with NAs that have a high genetic barrier to resistance, to counsel patients on medication adherence and to monitor virological breakthroughs. The recommended treatment for patients with chronic HCV infection is peg-IFN plus ribavirin that can decrease the occurrence of HCC in those who achieve a sustained virological response and have not yet progressed to cirrhosis. IFN-based treatment is reserved for patients with decompensated cirrhosis who are under evaluation of liver transplantation to reduce post-transplant recurrence of HCV. More effective therapeutic options such as direct acting antiviral agents will hopefully increase the response rate in difficult-totreat patients with HCV genotype 1. However, the risk of HCC remains in cirrhotic patients(both chronic HBV and HCV infection) if treatment is initiated after cirrhosis is established. Future research should focus on investigating new agents, especially for those patients with hepatic decompensation or post-transplantation. | Li-Ping Chen Jun Zhao Yan Du Yi-Fang Han Tong Su Hong-Wei Zhang Guang-Wen Cao | 2012 | World Journal of Virology2012，1，6： | 23 |
| 7 | Control of hepatitis B virus replication by interferons and Toll-like receptor signaling pathways显示文摘Hepatitis B virus(HBV) infection is one of the major causes of liver diseases, affecting more than 350 million people worldwide. The interferon(IFN)-mediated innate immune responses could restrict HBV replication at the different steps of viral life cycle. Indeed, IFN-α has been successfully used for treatment of patients with chronic hepatitis B. However, the role of the innate immune response in HBV replication and the mechanism of the anti-HBV effect of IFN-α are not completely explored. In this review, we summarized the currently available knowledge about the IFN-mediated anti-HBV effect in the HBV life cycle and the possible effectors downstream the IFN signaling pathway. The antiviral effect of Toll-like receptors(TLRs) in HBV replication is briefly discussed. The strategies exploited by HBV to evade the IFN- and TLR-mediated antiviral actions are summarized. | Rong-Juan Pei Xin-Wen Chen Meng-Ji Lu | 2014 | World Journal of Gastroenterology2014，20，33： | 21 |
| 8 | Risk for hepatocellular carcinoma in the course of chronic hepatitis B virus infection and the protective effect of therapy with nucleos(t)ide analogues显示文摘Hepatocellular carcinoma(HCC) is a major health problem worldwide, representing one of the leading causes of death. Chronic hepatitis B virus(HBV) infection(CHB) is the most important etiologic factor of this tumor, accounting for the development of more than50% of the cases in the world. Primary prevention ofHCC is possible by hepatitis B vaccination conferring protection from HBV infection. However, according to the World Health Organization Hepatitis B Fact sheet N° 204(update of July 2014) globally there exists a large pool of > 240 million people chronically infected with HBV who are at risk for development of HCC. These individuals represent a target population for secondary prevention both of cirrhosis and of HCC. Since ongoing HBV replication in CHB is linked with the progression of the underlying liver disease to cirrhosis as well as with the development of HCC, effective antiviral treatment in CHB has also been evaluated in terms of secondary prevention of HCC. Currently, most patients with active CHB are subjected to long term treatment with the first line nucleos(t)ide analogues entecavir and tenofovir. These compounds are of high antiviral potency and have a high barrier to HBV resistance compared to lamivudine, adefovir dipivoxil and even telbivudine. Many studies have shown that patients under antiviral treatment, especially those in virological remission, develop less frequently HCC compared to the untreated ones. However, the risk for development of HCC cannot be eliminated. Therefore, surveillance for the development of HCC of patients with chronic hepatitis B must be lifelong or until a time in the future when new treatments will be able to completely eradicate HBV from the liver particularly in the early stages of CHB infection. In this context, the aim of this review is to outline the magnitude of the risk for development of HCC among patients with CHB, in the various phases of the infection and in relation to virus, host and environmental factors as evaluated in the world literature. Moreover, the benefits of antiviral treatment of CHB with nucleos/tide analogs, which have changed the natural history of the disease and have reduced but not eliminated the risk of HCC are also reviewed. | Irene Rapti Stephanos Hadziyannis | 2015 | World Journal of Hepatology2015，7，8： | 20 |
| 9 | TRAF-mediated regulation of immune and inflammatory responses显示文摘The tumor necrosis factor (TNF) receptor-associated factor (TRAF) family consists of six mammalian members,and is shown to participate in signal transduction of a large number of receptor families including TNF receptor family (TNFR) and Toll-like receptors-interleukin-1 receptors (TLR-IL-1R) family.Upon receptor activation,TRAFs are directly or indirectly recruited to the intracellular domains of these receptors.They subsequently engage other signaling proteins to activate inhibitor of κB kinase (IKK) complex,TRAF family member-associated NF-κB activator (TANK)-binding kinase 1 (TBK1) and inducible I κB kinase (IKK-i) (also known as IKKε),ultimately leading to activation of transcription factors such as NF-κB and interferon-regulatory factor (IRF) to induce immune and inflammatory responses. | WANG YaYa1,ZHANG Peng2,LIU YingFang2 & CHENG GenHong1 1 Department of Microbiology,Immunology & Molecular Genetics,University of California Los Angeles,609 Charles E.Young Drive East,Los Angeles,California 90095,USA 2 National Laboratory of Biomacromolecules,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China | 2010 | Science China(Life Sciences)2010，53，2： | 19 |
| 10 | Combination of 'low-dose' ribavirin and interferon alfa-2a therapy followed by interferon alfa-2a monotherapy in chronic HCV-infected nonresponders and relapsers after interferon alfa-2a monotherapy显示文摘AIM To report on the efficacy, safety and tolerability of interferon alfa-2a combined with a 'low dose' of ribavirin for relapsers and non responders to alpha interferon monotherapy.METHODS Thirty-four chronic hepatitis C virus-infected non-responders to interferon alfa2a monotherapy (a course of at least 3 months treatment) and 13 relapsers to interferon alfa 2a monotherapy (a dose of 3 to 6 million units three times per week for at least 20 weeks but not more than 18 months) were treated with the same dose of interferon alfa-2a used before (3 to 6 million units three times per week) and ribavirin (10 mg/ kg daily) for 6 months. In complete responders, interferon alfa-2a was administered for further 6 months at the same dose used before as monotherapy.RESULTS Seven (20.6%) of 34 non-responders stopped the combined therapy due to adverse events, including two patients with histological and clinical Child A cirrhosis. In 17/27 (63%)non-responders, the combined therapy was stopped after three months because of non-response. Ten of the 27 non-responders completed the 1;2-month treatment course. At a mean follow up of 28 months (16- 37 months)after the treatment, 4/10 (15%) previous non-responders still remained complete responders,All 13 previous relapsers completed the 12-month treatment course. At a mean follow up of 22months (9 - 36 months) after treatment, 6/13(46%) the previous relapsers were stillsustained complete responders.CONCLUSION Our treatment schedule of the combined therapy for 6 months of interferon alfa2a with a low dose of ribavirin (10 mg/kg/day)followed by 6 months of interferon alfa-2amonotherapy is able to induce a sustainedcomplete response rate in 15% of non-responders and 46% of relapsers with chronic hepatitis C virus-related liver diseases comparable to those obtained with the standarddoses of ribavirin 1000 - 1200 mg/day.Randomized prospective controlled trials using lower total amounts of ribavirin in combination with interferon should be performed. | Perdita Wietzke-Braun Volker Meier Felix Braun Giuliano Ramadori | 2001 | World Journal of Gastroenterology2001，7，2： | 19 |
| 11 | Pegylated interferon α-2b up-regulates specific CD8+ T cells in patients with chronic hepatitis B显示文摘AIM:To investigate the effect of pegylated interferon (IFN) α-2b on specific CD8+ T lymphocytes in patients with chronic hepatitis B (CHB). METHODS:Twenty-one patients with CHB were treated with pegylated IFN α-2b. Periphery blood mononuclear cells were isolated from fresh heparinized blood by Ficoll-Hypaque density gradient centrifugation (density:1.077 g/L,Pharmingen) at weeks 0,4,8,12,and 24,respectively. Frequency of circulating hepatitis B virus (HBV) epitope-specific CD8 T cells was detected by flow cytometry. Cytokines were detected by cytometric bead assay. RESULTS:The frequency of circulating HBV core or env-specific CD8 T cells was higher (P < 0.05),the number of HBV core specific CD8 T cells was greater at week 24 (P < 0.05),the level of Th1-type cytokines [interleukin (IL)-12,tumor necrosis factor-α,and IFN-γ] was higher,while that of Th2-type cytokines (IL-4,IL-6,and IL-10) was lower in responders than in nonresponders (P < 0.05) after pegylated IFN α-2b treatment. The IL-6 level was correlated with HBV DNA (r = 0.597,P = 0.04),while the inducible protein-10 (IP-10) level was correlated with serum alanine aminotransferase (ALT) (r = 0.545,P = 0.005). The IP-10 level at week 8 after pegylated IFN α-2b treatment could predict the normalization of ALT in CHB patients (positive predict value = 56%,negative predict value = 92%). CONCLUSION:Pegylated IFN α-2b can enhance the immune response of CHB patients by increasing the frequency of HBV specific CD8+ T cells and regulating the Th1/Th2 cytokines. | Ji Chen,Yan Wang,Xue-Jie Wu,Jun Li,Feng-Qin Hou,Gui-Qiang Wang,Department of Infectious Diseases,Center for Liver Diseases,Peking University First Hospital,Beijing 100034,China | 2010 | World Journal of Gastroenterology2010，16，48： | 17 |
| 12 | Interferon therapy in hepatitis Cleading to chronic type 1 diabetes显示文摘AIM: To review the prevalence,clinical data and course of interferon-associated type 1 diabetes in chronic hepatitis C virus(HCV) infection.METHODS: Search of all interferon(INF)-related type 1diabetes mellitus(T1DM) cases published in the English literature from 1992 to December 2013 according to the key words: chronic hepatitis C infection,diabetes mellitus type 1,insulin dependent diabetes mellitus,and interferon treatment.We found 107 cases and analyzed their clinical and laboratory data and long-term followup.Due to the predominance of cases described in Japanese literature,we analyzed separately cases of Caucasian and Japanese origin.In addition we describe a representative case with HCV who developed INFrelated T1 DM.RESULTS: Our data show that INF treatment increases the risk of developing T1 DM by 10-18 fold compared with the corresponding general population and the median age of onset was 43 years(range: 24-66 years) in Caucasians and 52 years(range: 45-63 years) in Japanese.Most patients developed T1 DM during INF treatment,after a median time-period of 4.2 and 5.7 mo in Caucasian and Japanese groups,respectively.The clinical course was characterized by a fulminant course with abrupt severe hyperglycemia or ketoacidosis,a high titer of anti-islet autoantibodies and almost all patients(105/107) permanently required insulin therapy with a follow-up of up to 4 years.A substantial number of patients had evidence for other autoimmune disorders mainly thyroid diseases(25% and 31% in Caucasian and Japanese groups,respectively).CONCLUSION: INF-associated T1 DM in HCV has a fulminant course,often associated with other autoimmune diseases,and results almost inevitably in permanent insulin therapy requirement. | Taiba Zornitzki Stephen Malnick Lyudmila Lysyy Hilla Knobler | 2015 | World Journal of Gastroenterology2015，21，1： | 17 |
| 13 | Single-cell transcriptomic analysis defines the interplay between tumor cells,viral infection,and the microenvironment in nasopharyngeal carcinoma显示文摘Nasopharyngeal carcinoma(NPC)is an Epstein-Barr virus(EBV)-associated malignancy with a complex tumor ecosystem.How the interplay between tumor cells,EBV,and the microenvironment contributes to NPC progression and immune evasion remains unclear.Here we performed single-cell RNA sequencing on^104,000 cells from 19 EBV^+NPCs and 7 nonmalignant nasopharyngeal biopsies,simultaneously profiling the transcriptomes of malignant cells,EBV,stromal and immune cells.Overall,we identified global upregulation of interferon responses in the multicellular ecosystem of NPC.Notably,an epithelial–immune dual feature of malignant cells was discovered and associated with poor prognosis.Functional experiments revealed that tumor cells with this dual feature exhibited a higher capacity for tumorigenesis.Further characterization of the cellular components of the tumor microenvironment(TME)and their interactions with tumor cells revealed that the dual feature of tumor cells was positively correlated with the expression of co-inhibitory receptors on CD8^+tumor-infiltrating T cells.In addition,tumor cells with the dual feature were found to repress IFN-γproduction by T cells,demonstrating their capacity for immune suppression.Our results provide new insights into the multicellular ecosystem of NPC and offer important clinical implications. | Shanzhao Jin Ruoyan Li Ming-Yuan Chen Chao Yu Lin-Quan Tang Yan-Min Liu Jiang-Ping Li Yi-Na Liu Yi-Ling Luo Yifan Zhao Yu Zhang Tian-Liang Xia Shang-Xin Liu Qi Liu Guan-Nan Wang Rui You Jing-Yun Peng Jiang Li Feng Han Jianwei Wang Qiu-Yan Chen Li Zhang Hai-Qiang Mai Benjamin E.Gewurz Bo Zhao Lawrence S.Young Qian Zhong Fan Bai Mu-Sheng Zeng | 2020 | Cell Research2020，30，11： | 16 |
| 14 | High-level disinfection of gastrointestinal endoscope reprocessing显示文摘High level disinfection(HLD) of the gastrointestinal(GI)endoscope is not simply a slogan, but rather is a form of experimental monitoring-based medicine. By definition,GI endoscopy is a semicritical medical device. Hence,such medical devices require major quality assurance for disinfection. And because many of these items are temperature sensitive, low-temperature chemical methods, such as liquid chemical germicide, must be used rather than steam sterilization. In summarizing guidelines for infection prevention and control for GI endoscopy, there are three important steps that must be highlighted: manual washing, HLD with automated endoscope reprocessor, and drying. Strict adherence to current guidelines is required because compared to any other medical device, the GI endoscope is associated with more outbreaks linked to inadequate cleaning or disinfecting during HLD. Both experimental evaluation on the surveillance bacterial cultures and in-use clinical results have shown that, the monitoring of the stringent processes to prevent and control infection is an essential component of the broader strategy to ensure the delivery of safe endoscopy services, because endoscope reprocessing is a multistep procedure involving numerous factors that can interfere with its efficacy. Based on our years of experience in the surveillance of culture monitoring of endoscopic reprocessing, we aim in this study to carefully describe what details require attention in the GI endoscopy disinfection and to share our experience so that patients can be provided with high quality and safe medical practices. Quality management encompasses all aspects of pre- and postprocedural care including the efficiency of the endoscopy unit and reprocessing area, as well as the endoscopic procedure itself. | King-Wah Chiu Lung-Sheng Lu Shue-Shian Chiou | 2015 | World Journal of Experimental Medicine2015，5，1： | 13 |
| 15 | Models for predicting hepatitis B e antigen seroconversion in response to interferon-α in chronic hepatitis B patients显示文摘AIM:To develop models to predict hepatitis B e antigen(HBe Ag)seroconversion in response to interferon(IFN)-αtreatment in chronic hepatitis B patients.METHODS:We enrolled 147 treatment-nave HBe Agpositive chronic hepatitis B patients in China and analyzed variables after initiating IFN-α1b treatment.Patients were tested for serum alanine aminotransferase(ALT),hepatitis B virus-DNA,hepatitis B surface antigen(HBs Ag),antibody to hepatitis B surface antigen,HBe Ag,antibody to hepatitis B e antigen(anti-HBe),and antibody to hepatitis B core antigen(anti-HBc)at baseline and 12 wk,24 wk,and 52 wk after initiating treatment.We performed univariate analysis to identify response predictors among the variables.Multivariate models to predict treatment response were constructed at baseline,12 wk,and 24 wk.RESULTS:At baseline,the 3 factors correlating most with HBe Ag seroconversion were serum ALT level>4×the upper limit of normal(ULN),HBe Ag≤500 S/CO,and anti-HBc>11.4 S/CO.At 12 wk,the 3 factors most associated with HBe Ag seroconversion were HBe Ag level≤250 S/CO,decline in HBe Ag>1 log10 S/CO,and anti-HBc>11.8 S/CO.At 24 wk,the 3 factors most associated with HBe Ag seroconversion were HBe Ag level≤5 S/CO,anti-HBc>11.4 S/CO,and decline in HBe Ag>2 log10 S/CO.Each variable was assigned a score of1,a score of 0 was given if patients did not have any of the 3 variables.The 3 factors most strongly correlating with HBe Ag seroconversion at each time point were used to build models to predict the outcome after IFN-αtreatment.When the score was 3,the response rates at the 3 time points were 57.7%,83.3%,and 84.0%,respectively.When the score was 0,the response rates were 2.9%,0.0%,and 2.1%,respectively.CONCLUSION:Models with good negative and positive predictive values were developed to calculate the probability of response to IFN-αtherapy. | Chang-Tai Wang Ya-Fei Zhang Bing-Hu Sun Yu Dai Hui-Lan Zhu Yuan-Hong Xu Meng-Ji Lu Dong-Liang Yang Xu Li Zhen-Hua Zhang | 2015 | World Journal of Gastroenterology2015，21，18： | 12 |
| 16 | Hepatitis C virus infection and thyroid autoimmunedisorders:A model of interactions between the host and theenvironment显示文摘The hepatitis C virus(HCV) infection is an important public health problem and it is associated with hepatic and extrahepatic manifestations. Autoimmune thyroid diseases are common in HCV infected patients and the standard interferon-based treatment is associated with an increase of the immune-mediated thyroid damage. Recent evidence in the literature analyzed critical points of the mechanisms of thyroid damage, focusing on the balance between the two sides of the interaction: The environment(virus infection with potential crossreaction) and the host(susceptibility genes with consistent immune response). The spectrum of antiviral treatment for chronic HCV infection is rapidly expanding for the development of dual o triple therapy. The availability of interferon-free combined treatment with direct antiviral agents for HCV is very promising, in order to ameliorate the patient compliance and to reduce the development of thyroid autoimmunity. | francesca pastore antonio martocchia manuela stefanelli pietro prunas stefania giordano lavinia toussan antonio devito paolo falaschi | 2016 | World Journal of Hepatology2016，8，2： | 12 |
| 17 | Progression and status of antiviral monitoring in patients with chronic hepatitis B:From HBsAg to HBV RNA显示文摘As alternative indexes of hepatitis B virus(HBV),co-valently closed circular DNA(cccDNA) transcriptional activity,hepatitis B surface antigen(HBsAg),hepatitis B core-related antigen(HBcrAg),and peripheral blood RNA known as pgRNA,have been advocated as novel serum markers for prediction of prognosis and treatment response in chronic hepatitis B(CHB). Since the availability of commercial quantitative assays of HBsAg in 2011,HBsAg has been widely used for predicting treatment response of patients with CHB. Patients who received interferon therapy have shown a sharper reduction of HBsAg level than those who received nucleoside drug(NAs) therapy. Upon peginterferon treatment,sustained responders have presented a larger reduction of HBsAg level than the non-responders. An absence of HBsAg decline,together with < 2 log reduction in HBV DNA at week 12,can serve as a stopping rule in HBsAg-negative patients infected with genotype D HBV. A sharp reduction of HBs Ag titer in the NAs therapy is a predictor of HBsAg clearance in long-term treatment. HBcrAg,which consists of three species of related proteins sharing an identical 149 amino acid sequence,including HbcAg,hepatitis B e antigen(HBeAg),and a truncated 22-kDa precore protein,is still detectable in situations where serum HBV DNA levels become undetectable or HBsAg loss is achieved. Therefore,HBcrAg remains a measurable serum marker to correlate with cccDNA in this situation. The decline in HBcrAg has been observed with NAs therapy and the pattern of decline might provide prognostic information on the risk of HBV posttreatment reactivation. Peripheral blood RNA,which is known as pgRNA,directly derives from cccDNA and reflects intrahepatic cccDNA level. Quantitative pgRNA has been suggested to be helpful in CHB management. However,commercial quantitative assays are lacking. Additionally,the use of simultaneous and continuous clearance of HBV RNA and HBV DNA in serum has been suggested to be a safe stopping rule of NAs therapy for patients with CHB. However,clinical studies of large sample sizes are needed to prove the feasibility andsignificance of using serum HBV RNA as the assessment standard of antiviral therapy in CHB and the safety of the stopping rule in clinics. | Ya-Yun Liu Xue-Song Liang | 2018 | World Journal of Hepatology2018，10，9： | 12 |
| 18 | Anti-viral therapy to reduce recurrence and improve survival in hepatitis B virus-related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC)is the most common malignancy and the third leading cause of cancer death worldwide.Chronic infection with hepatitis B virus(HBV)and hepatitis C virus accounts for approximately75%-80%of HCC cases worldwide.In particular,chronic HBV infection is a predominant risk factor for HCC in Asia and Africa.Hepatic resection and radiofrequency ablation are increasingly used for the curative treatment of HCC,and good local control can be achieved.However,the high rate of recurrence is a major obstacle to improving prognosis.A high viral load of HBV DNA is the most important correctable risk factor for recurrence.Furthermore,interferon and/or nucleotide analogues may decrease HBV DNA.Therefore,these drugs may decrease recurrence.In this article,treatment strategies for HBV-related HCC are described in order to reduce recurrence and improve survival. | Toru Ishikawa | 2013 | World Journal of Gastroenterology2013，19，47： | 11 |
| 19 | Antiviral therapy for chronic hepatitis B: Combination of nucleoside analogs and interferon显示文摘The ideal goal of chronic hepatitis B(CHB) treatment should be suppression of emergence of hepatocellular carcinoma through the disappearance of hepatitis B s antigen(HBs Ag) rather than the control of serum hepatitis B virus-DNA level. For this purpose, various types of combination therapies using nucleoside analogs(NAs) and interferon(IFN) have been conducted. The therapeutic effects of combination of two different kinds of agents are better than those of the monotherapy using NAs or IFN alone, probably because different pharmaceutical properties might act in a coordinated manner. Recently, combination therapies with NAs and IFN and sequential therapies with NAs administration followed by IFN therapy have been routinely employed. We previously reported that combination therapy using entecavir(ETV) and pegylated(PEG)-IFN showed antiviral effects in 71% of CHB patients; the effect of this combination was better than that using lamivudine(LAM) and PEG-IFN. This is partially explained by the better antiviral effects of ETV than those of LAM. In our analysis, the cohort of CHB consisted of the patients who showed a flare-up of hepatitis before antiviral therapy, and their baseline HBs Ag levels were relatively low. Therefore, in addition to the combination of the agents, the appropriate selection of patients is critical to achieve a good viral response. | Satoru Hagiwara Naoshi Nishida Masatoshi Kudo | 2015 | World Journal of Hepatology2015，7，23： | 11 |
| 20 | Inflammation and tumor progression:signaling pathways and targeted intervention显示文摘Cancer development and its response to therapy are regulated by inflammation,which either promotes or suppresses tumor progression,potentially displaying opposing effects on therapeutic outcomes.Chronic inflammation facilitates tumor progression and treatment resistance,whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells(DCs)and antigen presentation,leading to anti-tumor immune responses.In addition,multiple signaling pathways,such as nuclear factor kappa B(NF-kB),Janus kinase/signal transducers and activators of transcription(JAK-STAT),toll-like receptor(TLR)pathways,cGAS/STING,and mitogen-activated protein kinase(MAPK);inflammatory factors,including cytokines(e.g.,interleukin(IL),interferon(IFN),and tumor necrosis factor(TNF)-a),chemokines(e.g.,C-C motif chemokine ligands(CCLs)and C-X-C motif chemokine ligands(CXCLs)),growth factors(e.g.,vascular endothelial growth factor(VEGF),transforming growth factor(TGF)-P),and inflammasome;as well as inflammatory metabolites including prostaglandins,leukotrienes,thromboxane,and specialized proresolving mediators(SPM),have been identified as pivotal regulators of the initiation and resolution of inflammation.Nowadays,local irradiation,recombinant cytokines,neutralizing antibodies,small-molecule inhibitors,DC vaccines,oncolytic viruses,TLR agonists,and SPM have been developed to specifically modulate inflammation in cancer therapy,with some of these factors already undergoing clinical trials.Herein,we discuss the initiation and resolution of inflammation,the crosstalk between tumor development and inflammatory processes.We also highlight potential targets for harnessing inflammation in the treatment of cancer. | Huakan Zhao Lei Wu Guifang Yan Yu Chen Mingyue Zhou Yongzhong Wu Yongsheng Li | 2021 | Signal Transduction and Targeted Therapy2021，6，8： | 11 |
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