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世界胃肠病学杂志（英文版）
世界胃肠病学杂志（英文版）

潘伯荣

周刊

1007-9327

wjg@wjgnet.com

010-85381901-628

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北京市朝阳区东四环中路62号楼远洋国际中心D座903室

世界胃肠病学杂志（英文版）/Journal World Journal of GastroenterologyCSCDCSTPCDSCI
查看更多>>主要报道和刊登国内外、特别是我国消化病学者具有创造性的、有较高学术水平的基础和临床研究论文、研究快报等. 对具有中国特色的研究论文, 如食管癌、胃癌、肝癌、大肠癌、病毒性肝炎、幽门螺杆菌、中医中药、中西医结合和基于作者自己研究工作为主的综述性论文, 将优先发表. 读者对象为基础研究或临床研究的消化专业工作者。
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    Risk for gastric neoplasias in patients with chronic atrophic gastritis: A critical reappraisal

    Lucy VannellaEdith LahnerBruno Annibale
    1279-1285页
    查看更多>>摘要：Chronic atrophic gastritis (CAG) is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue (non-metaplastic atrophy) or by glandular structures inappropriate for location (metaplastic atrophy).Epidemiological data suggest that CAG is associated with two different types of tumors:Intestinal-type gastric cancer (GC) and type Ⅰ gastric carcinoid (T I GC).The pathophysiological mechanisms which lead to the development of these gastric tumors are different.It is accepted that a multistep process initiating from Helicobacterpylori-related chronic inflammation of the gastric mucosa progresses to CAG,intestinal metaplasia,dysplasia and,finally,leads to the development of GC.The T I GC is a gastrin-dependent tumor and the chronic elevation of gastrin,which is associated with CAG,stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of T I GC.Thus,several events occur in the gastric mucosa before the development of intestinal-type GC and/or T I GC and these take several years.Knowledge of CAG incidence from superficial gastritis,its prevalence in different clinical settings and possible risk factors associated with the progression of this condition to gastric neoplasias are important issues.This editorial intends to provide a brief review of the main studies regarding incidence and prevalence or CAG and risk factors for the development of gastric neoplasias.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Mouse models of pancreatic cancer

    Marta Herreros-VillanuevaElizabeth HijonaAngel CosmeLuis Bujanda...
    1286-1294页
    查看更多>>摘要：Pancreatic cancer is one of the most lethal of human malignancies ranking 4th among cancer-related death in the western world and in the United States,and potent therapeutic options are lacking.Although during the last few years there have been important advances in the understanding of the molecular events responsible for the development of pancreatic cancer,currently specific mechanisms of treatment resistance remain poorly understood and new effective systemic drugs need to be developed and probed.In vivo models to study pancreatic cancer and approach this issue remain limited and present different molecular features that must be considered in the studies depending on the purpose to fit special research themes.In the last few years,several genetically engineered mouse models of pancreatic exocrine neoplasia have been developed.These models mimic the disease as they reproduce genetic alterations implicated in the progression of pancreatic cancer.Genetic alterations such as activating mutations in KRas,or TGFb and/or inactivation of tumoral suppressors such as p53,INK4A/ARF BRCA2 and Smad4 are the most common drivers to pancreatic carcinogenesis and have been used to create transgenic mice.These mouse models have a spectrum of pathologic changes,from pancreatic intraepithelial neoplasia to lesions that progress histologically culminating in fully invasive and metastatic disease and represent the most useful preclinical model system.These models can characterize the cellular and molecular pathology of pancreatic neoplasia and cancer and constitute the best tool to investigate new therapeutic approaches,chemopreventive and/or anticancer treatments.Here,we review and update the current mouse models that reproduce different stages of human pancreatic ductal adenocarcinoma and will have clinical relevance in future pancreatic cancer developments.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Magnifying endoscopy in upper gastroenterology for assessing lesions before completing endoscopic removal

    Ning-Li ChaiEn-Qiang Ling-HuYoshinori MoritaDaisuke Obata...
    1295-1307页
    查看更多>>摘要：Any prognosis of gastrointestinal (GI) cancer is closely related to the stage of the disease at diagnosis.Endoscopic submucosal dissection (ESD) and en bloc endoscopic mucosal resection (EMR) have been performed as curative treatments for many early-stage GI lesions in recent years.The technologies have been widely accepted in many Asian countries because they are minimally invasive and supply thorough histopathologic evaluation of the specimens.However,before engaging in endoscopic therapy,an accurate diagnosis is a precondition to effecting the complete cure of the underlying malignancy or carcinoma in situ.For the past few years,many new types of endoscopic techniques,including magnifying endoscopy with narrow-band imaging (MENBI),have emerged in many countries because these methods provide a strong indication of early lesions and are very useful in determining treatment options before ESD or EMR.However,to date,there is no comparable classification equivalent to "Kudo's Pit Pattern Classification in the colon",for the upper GI,there is still no clear internationally accepted classification system of magnifying endoscopy.Therefore,in order to help unify some viewpoints,here we will review the defining optical imaging characteristics and the current representative classifications of microvascular and microsurface patterns in the upper GI tract under ME-NBI,describe the accurate relationship between them and the pathological diagnosis,and their clinical applications prior to ESD or en bloc EMR.We will also discuss assessing the differentiation and depth of invasion,defying the lateral spread of involvement and targeting biopsy in real time.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Probiotic modulation of dendritic cells co-cultured with intestinal epithelial cells

    Ji Yeun KimMyeong Soo ParkGeun Eog Ji
    1308-1318页
    查看更多>>摘要：AIM:TO investigate cytokine production and cell surface phenotypes of dendritic cells (DC) in the presence of epithelial cells stimulated by probiotics.METHODS:Mouse DC were cultured alone or together with mouse epithelial cell monolayers in normal or inverted systems and were stimulated with heat-killed probiotic bacteria,Bifidobacteriumlactis AD011 (BL),Bifidobacterium bifidum BGN4 (BB),Lactobacillus casei IBS041 (LC),and Lactobacillus acidophilus AD031 (LA),for 12 h.Cytokine levels in the culture supernatants were determined by enzyme-linked immunosorbent assay and phenotypic analysis of DC was investigated by flow cytometry.RESULTS:BB and LC in single-cultured DC increased the expression of I-Ad,CD86 and CD40 (I-Ad,18.51 vs 30.88,46.11; CD86,62.74 vs 92.7,104.12; CD40,0.67vs 6.39,3.37,P ＜ 0.05).All of the experimental probiotics increased the production of inflammatory cytokines,interleukin (IL)-6 and tumor necrosis factor (TNF)-α.However,in the normal co-culture systems,LC and LA decreased the expression of I-Ad (39.46 vs 30.32,33.26,P ＜ 0.05),and none of the experimental probiotics increased the levels of IL-6 or TNF-α.In the inverted coculture systems,LC decreased the expression of CD40 (1.36 vs-2.27,P ＜ 0.05),and all of the experimental probiotics decreased the levels of IL-6.In addition,BL increased the production of IL-10 (103.8 vs 166.0,P＜ 0.05) and LC and LA increased transforming growth factor-3 secretion (235.9 vs 618.9,607.6,P ＜ 0.05).CONCLUSION:These results suggest that specific probiotic strains exert differential immune modulation mediated by the interaction of dendritic cells and epithelial cells in the homeostasis of gastrointestinal tract.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Enhancement of CTLs induced by DCs loaded with ubiquitinated hepatitis B virus core antigen

    Jian-Hua ChenYong-Sheng YuXiao-Hua ChenHong-Hong Liu...
    1319-1327页
    查看更多>>摘要：AIM:TO investigate whether hepatitis B virus (HBV) could induce a hepatitis B virus core antigen (HBcAg)-specific cytotoxic T lymphocyte (CTL) response in vitro by dendritic cells (DCs) transduced with lentiviral vector-encoding ubiquitinated hepatitis B virus core antigen (LV-Ub-HBcAg).METHODS:Recombinant LV-Ub-HBcAg were transfected into highly susceptible 293 T cells to obtain high virus titres.Bone marrow-derived DCs isolated from BALB/c mice were cultured with recombinant granulocyte-macrophage colony-stimulating factor and recombinant interleukin (IL)-4.LV-Ub-HBcAg,lentiviral vector-encoding hepatitis B virus core antigen (LV-HBcAg),lentiviral vector (LV) or lipopolysaccharide were added to induce DC maturation,and the DC phenotypes were analyzed by flow cytometry.The level of IL-12 in the supernatant was detected by enzyme-linked immunosorbent assay (ELISA).T lymphocytes were proliferated using Cell Counting Kit-8.DCs were cultured and induced to mature using different LVs,and co-cultured with allogeneic T cells to detect the secretion levels of IL-2,IL-4,IL-10 and interferon-γ in the supernatants of T cells by ELISA.Intracellular cytokines of proliferative T cells were analyzed by flow cytometry,and specific CTL activity was measured by a lactate dehydrogenase release assay.RESULTS:LV-Ub-HBcAg-induced DCs secreted more IL-12 and upregulated the expression of CD80,CD86 and major histocompatibility class Ⅱ.DCs sensitised by different LVs effectively promoted cytokine secretion;the levels of IL-2 and interferon-γ induced by LV-Ub-HBcAg were higher than those induced by LV-HBcAg.Compared with LV-HBcAg-transduced DCs,LV-Ub-HBcAg-transduced DCs more efficiently stimulated the proliferation of T lymphocytes and generated HBcAg-specific cytotoxic T lymphocytes.CONCLUSION:LV-Ub-HBcAg effectively induced DC maturation.The mature DCs efficiently induced T cell polarisation to Th1 and generated HBcAg-specific CTLs.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Loss of Wnt5a and Ror2 protein in hepatocellular carcinoma associated with poor prognosis

    Ming GengYong-Cheng CaoYing-Jian ChenHui Jiang...
    1328-1338页
    查看更多>>摘要：AIM:To investigate the expression and clinical significance of Wnt member 5a (Wnt5a) and receptor tyrosine kinase-like orphan receptor 2 (Ror2) in hepatocellular carcinoma (HCC).METHODS:In HCC tissues obtained from 85 patients,the protein expressions of Wnt5a,Ror2,β-catenin,and Ki-67 via immunohistochemical staining using the Envision Plus System.The antibody binding was visualized with 3,3'-diaminobenzidine tetrahydrochloride (DAB) before brief counterstaining with Mayer's hematoxylin.The degree of immunohistochemical staining was recorded using a semiquantitative and subjective grading system.The mRNA expression of Ror2 was examined by real-time reverse transcription polymerase chain reaction,including nineteen of the 85 HCC and three normal liver tissues.The ratios of Ror2 to the housekeeping gene GAPDH represented the normalized relative levels of Ror2 expression.To determine the prognostic factor,the outcome of the 82 patients was determined by reviewing their medical charts.The overall and disease-free survival rates were estimated using the Kaplan-Meier method and compared with the log-rank test.The prognostic analysis was carried out with univariate and multivariate Cox regressions models.RESULTS:Compared to nontumorous (hepatitis or cirrhotic) tissues,Ror2 mRNA expression was clearly decreased in HCC.Ror2 and Wnt5a protein expressions in the majority of HCC patients (63％ and 77％,respectively) was significantly less in tumor tissues,as compared to adjacent nontumorous tissues,and this reduction was correlated with increasing serum α-fetoprotein and tumor stage.In 68％ (58/85) of the HCC cases,the expression of β-catenin in tumor tissues was either downregulated in the cellular membrane,upregulated in the cytoplasm,or both.Survival analysis indicated that Wnt5a and Ror2 protein expressions could be regarded as independent prognostic factors for HCC; HCC patients with decreased Wnt5a or Ror2 protein expression had a poorer prognosis than those with elevated Wnt5a and Ror2 expression (P =0.016,P =0.007,respectively).CONCLUSION:Wnt5a and Ror2 may serve as tumor suppressor genes in the development of HCC,and may serve as clinicopathologic biomarkers for prognosis in HCC patients.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Chronic hepatitis C: Treat or wait? Medical decision making in clinical practice

    Claus NiederauDietrich HüppeElmar ZehnterBernd M(o)ller...
    1339-1347页
    查看更多>>摘要：AIM:To analyzes the decision whether patients with chronic hepatitis C virus (HCV) infection are treated or not.METHODS:This prospective cohort study included 7658 untreated patients and 6341 patients receiving pegylated interferon α2a/ribavirin,involving 434 physicians/institutions throughout Germany (377 in private practice and 57 in hospital settings).A structured questionnaire had to be answered prior to the treatment decision,which included demographic data,information about the personal life situation of the patients,anamnesis and symptomatology of hepatitis C,virological data,laboratory data and data on concomitant diseases.A second part of the study analyzes patients treated with pegylated interferon α2a.All questionnaires included reasons against treatment mentioned by the physician.RESULTS:Overall treatment uptake was 45％.By multivariate analysis,genotype 1/4/5/6,HCV-RNA ≤ 520 000 IU/mL,normal alanine aminotransferase (ALT),platelets ≤ 142 500/μL,age ＞ 56 years,female gender,infection length ＞ 12.5 years,concomitant diseases,human immunodeficiency virus co-infection,liver biopsy not performed,care in private practice,asymptomatic disease,and unemployment were factors associated with reduced treatment rate.Treatment and sustained viral response rates in migrants (1/3 of cohort) were higher than in German natives although 1/3 of migrants had language problems.Treatment rate and liver biopsy were higher in clinical settings when compared to private practice and were low when ALT and HCV-RNA were low.CONCLUSION:Some reasons against treatment were medically based whereas others were related to fears,socio-economical problems,and information deficits both on the side of physicians and patients.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Celiac disease: Management of persistent symptoms in patients on a gluten-free diet

    David H DewarSuzanne C DonnellySimon D McLaughlinMatthew W Johnson...
    1348-1356页
    查看更多>>摘要：AIM:To investigate all patients referred to our center with non-responsive celiac disease (NRCD),to establish a cause for their continued symptoms.METHODS:We assessed all patients referred to our center with non-responsive celiac disease over an 18-mo period.These individuals were investigated to establish the eitiology of their continued symptoms.The patients were first seen in clinic where a thorough history and examination were performed with routine blood work including tissue transglutaminase antibody measurement.They were also referred to a specialist gastroenterology dietician to try to identift any lapses in the diet and sources of hidden gluten ingestion.A repeat small intestinal biopsy was also performed and compared to biopsies from the referring hospital where possible.Colonoscopy,lactulose hydrogen breath testing,pancreolauryl testing and computed tomography scan of the abdomen were undertaken if the symptoms persisted.Their clinical progress was followed over a minimum of 2 years.RESULTS:One hundred and twelve consecutive patients were referred with NRCD.Twelve were found not to have celiac disease (CD).Of the remaining 100 patients,45％ were not adequately adhering to a strict gluten-free diet,with 24 (53％) found to be inadvertently ingesting gluten,and 21 (47％) admitting noncompliance.Microscopic colitis was diagnosed in 12％ and small bowel bacterial overgrowth in 9％.Refractory CD was diagnosed in 9％.Three of these were diagnosed with intestinal lymphoma.After 2 years,78 patients remained well,eight had continuing symptoms,and four had died.CONCLUSION:In individuals with NRCD,a remediable cause can be found in 90％:with continued gluten ingestion as the leading cause.We propose an algorithm for investigation.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Second-line therapy for gemcitabine-pretreated advanced or metastatic pancreatic cancer

    Romain AltweggMarc YchouVanessa GuillaumonSimon Thezenas...
    1357-1364页
    查看更多>>摘要：AIM:To investigate second-line chemotherapy in gemcitabine-pretreated patients with advanced or metastatic pancreatic cancer [(frequency,response,outcome,course of carbohydrate antigen 19-9 (CA 19-9)].METHODS:This retrospective study included all patients with advanced or metastatic pancreatic cancer (adenocarcinoma or carcinoma) treated with secondline chemotherapy in our center between 2000 and 2008.All patients received first-line chemotherapy with gemcitabine,and prior surgery or radiotherapy was permitted.We analyzed each chemotherapy protocol for second-line treatment,the number of cycles and the type of combination used.The primary endpoint was overall survival.Secondary endpoints included progression-free survival,response rate,grade 3-4 toxicity,dosage modifications and CA 19-9 course.RESULTS:A total of eighty patients (38％) underwent a second-line therapy among 206 patients who had initially received first-line treatment with a gemcitabine-based regimen.Median number of cycles was 4 (range:1-12) and the median duration of treatment was 2.6 mo (range:0.3-7.4).The overall disease control rate was 40.0％.The median overall survival and progression-free survival from the start of second-line therapy were 5.8 (95％ CI:4.1-6.6) and 3.4 mo (95％ CI:2.4-4.2),respectively.Toxicity was generally acceptable.Median overall survival of patients with a CA 19-9 level declining by more than 20％ was 10.3 mo (95％ CI:4.5-11.6) vs 5.2 mo (95％ CI:4.0-6.4) for others (P =0.008).CONCLUSION:A large proportion of patients could benefit from second-line therapy,and CA 19-9 allows efficient treatment monitoring both in first and secondline chemotherapy.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普

    Post-cholecystectomy symptoms were caused by persistence of a functional gastrointestinal disorder

    Malte SchmidtKarl S(o)ndenaaJohn A DumotSteven Rosenblatt...
    1365-1372页
    查看更多>>摘要：AIM:To classify gallstone disease as a basis for assessment of post-cholecystectomy symptoms.METHODS:One hundred and fifty three patients with a clinical and ultrasonographic diagnosis of gallstones filled out a structured questionnaire on abdominal pain symptoms and functional gastrointestinal disorder (FGID) before and at six months after cholecystectomy.Symptom frequency groups (SFG) were categorized according to frequency of pain attacks.According to certain pain characteristics in gallstone patients,a gallstone symptom score was accorded on a scale from one to ten.A visual analogue scale was used to quantify pain.Operative specimens were examined for size and magnitude of stone contents as well as presence of bacteria.Follow-up took place after six months with either a consultation or via a mailed questionnaire.Resuits were compared with those obtained pre-operatively to describe and analyze symptomatic outcome.RESULTS:SFG groups were categorized as severe (24.2％),moderate (38.6％),and mild (22.2％) attack frequency,and a chronic pain condition (15％).Pain was cured or improved in about 90％ of patients and two-thirds of patients obtained complete symptom relief.Patients with the most frequent pain episodes were less likely to obtain symptom relief.FGID was present in 88％ of patients pre-operatively and in 57％ postoperatively (P =0.244).Those that became asymptomatic or improved with regard to pain also had most relief from FGID (P =0.001).No pre-operative FGID meant almost complete cure.CONCLUSION:Only one third of patients with FGID experienced postoperative relief,indicating that FGID was a dominant cause of post-cholecystectomy symptoms.
      原文链接:
    • NETL
    • NSTL
    • 万方数据
    • 维普