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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

100025

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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    Pentoxifylline in hepatopulmonary syndrome

    Hamid Reza KianifarMaryam KhalesiEftekhar MahmoodiMonavar Afzal Aghaei...
    4912-4916页
    查看更多>>摘要:AIM:To determine the effects of pentoxifylline (PTX)on clinical manifestations and evaluate arterial blood gas data in hepatopulmonary syndrome (HPS) in children.METHODS:In a pilot study of 10 children with chronic liver disease,who had HPS,20 mg/kg/d PTX was administered for 3 mo.Clinical data and arterial blood gas parameters were evaluated at baseline,the end of the treatment period,and 3 mo after drug discontinuation.RESULTS:Six patients could tolerate PTX,while four patients experienced complications.Among patients who could tolerate PTX,there was a significant increase in arterial oxygen pressure (PaO2) (P =0.02) and oxygen saturation (SaO2) (P =0.04) and alveolar-arterial oxygen gradient (P =0.02) after 3 mo of treatment.Significant decreases in PaO2 (P =0.02) and alveolararterial oxygen gradient (P =0.02) were also seen after drug discontinuation.CONCLUSION:PTX may improve PaO2,SaO2 and alveolar-arterial oxygen gradient in the early stage of HPS.

    Inducible nitric oxide synthetase genotype and Helicobacter pylori infection affect gastric cancer risk

    Alireza RafieiVahid HosseiniGhasern JanbabaiBahman Fazli...
    4917-4924页
    查看更多>>摘要:AIM:To investigate the association of the inducible nitric oxide synthetase (iNOS) C150T polymorphism with Helicobacter pylori (H.pylorl) infection and gastric cancer (GC) risk in Iran.METHODS:In order to determine whether there was a correlation between iNOS genotype and GC in Iran,we conducted a case-control study using samples from 329 individuals.For each sample,the C150T iNOS polymorphism was genotyped by polymerase chain reaction (PCR) and restriction digestion.Patients were grouped by cancer presence,demographic and behavior characteristics,and H.pylori infection status.Statistical tests were conducted to determine whether any behavioral factors or a particular iNOS genotype was associated with GC in the study population.RESULTS:In this population,we found that smoking,hot beverage consumption,a familial history of GC and H.pylori infection status were significantly associated with GC development (P =0.015,P < 0.001,P =0.0034,and P < 0.015,respectively).The distribution of the C150T iNOS genotypes among the two study groups was not statistically significant alone,but was impacted by H.pylori infection status.When compared to the non-H,pylori infected group,cancer patients who had a heterozygous CT genotype and were also infected with H.pylori were 2.1 times more at risk of developing GC [odds ratio (OR) =2.1,P =0.03] while those with a homozygous (TT) genotype and infected with H.pylori were 5.0 times more at risk of developing GC (OR =5.0,P =0.029).In contrast,this association was not seen in patients in the control group.CONCLUSION:A CT or TT polymorphism at position 150 in the iNOS gene significantly increases the risk of GC and may be a marker for GC susceptibility.

    Endothelial precursor cells promote angiogenesis in hepatocellular carcinoma

    Xi-Tai SunXian-Wen YuanHai-Tao ZhuZheng-Ming Deng...
    4925-4933页
    查看更多>>摘要:AIM:To investigate the role of bone marrow-derived endothelial progenitor cells (EPCs) in the angiogenesis of hepatocellular carcinoma (HCC).METHODS:The bone marrow of HCC mice was reconstructed by transplanting green fluorescent protein (GFP) + bone marrow cells.The concentration of circulating EPCs was determined by colony-forming assays and fluorescence-activated cell sorting.Serum and tissue levels of vascular endothelial growth factor (VEGF)and colony-stimulating factor (CSF) were quantified by enzyme-linked immunosorbent assay.The distribution of EPCs in tumor and tumor-free tissues was detected by immunohistochemistry and real-time polymerase chain reaction.The incorporation of EPCs into hepatic vessels was examined by immunofluorescence and immunohistochemistry.The proportion of EPCs in vessels was then calculated.RESULTS:The HCC model was successful established.The flow cytometry analysis showed the mean percentage of CD133CD34 and CD133VEGFR2 double positive cells in HCC mice was 0.45% ± 0.16% and 0.20% ±0.09% respectively.These values are much higher than in the sham-operation group (0.11% ± 0.13%,0.05%± 0.11%,n =9) at 14 d after modeling.At 21 d,the mean percentage of circulating CD133CD34 and CD-133VEGFR2 cells is 0.23% ± 0.19%,0.25% ± 0.15%in HCC model vs 0.05% ± 0.04%,0.12% ± 0.11% in control.Compared to the transient increase observed in controls,the higher level of circulating EPCs were induced by HCC.In addition,the level of serum VEGF and CSF increased gradually in HCC,reaching its peak 14 d after modeling,then slowly decreased.Consecutive sections stained for the CD133 and CD34 antigens showed that the CD133+ and CD34+ VEGFR2 cells were mostly recruited to HCC tissue and concentrated in tumor microvessels.Under fluorescence microscopy,the bone-marrow (BM)-derived cells labeled with GFP were concentrated in the same area.The relative levels of CD133 and CD34 gene expression were elevated in tumors,around 5.0 and 3.8 times that of the tumor free area.In frozen liver sections from HCC mice,cells co-expressing CD133 and VEGFR2 were identified by immunohistochemical staining using anti-CD133 and VEGFR2 antibodies.In tumor tissue,the double-positive cells were incorporated into vessel walls.In immunofluorescent staining.These CD31 and GFP double positive cells are direct evidence that tumor vascular endothelial cells (VECs) come partly from BM-derived EPCs.The proportion of GFP CD31 double positive VECs (out of all VECs) on day 21 was around 35.3%± 21.2%.This is much higher than the value recorded on day 7 group (17.1% ± 8.9%).The expression of intercellular adhesion molecule 1,vascular adhesion molecule 1,and VEGF was higher in tumor areas than in tumor-free tissues.CONCLUSION:Mobilized EPCs were found to participate in tumor vasculogenesis of HCC.Inhibiting EPC mobilization or recruitment to tumor tissue may be an efficient strategy for treating HCC.

    Coexistence of hyperlipidemia and acute cerebral ischemia/reperfusion induces severe liver damage in a rat model

    Wei-Hong GongWen-Xia ZhengJun WangShi-Hui Chen...
    4934-4943页
    查看更多>>摘要:AIM:To investigate the correlation of hyperlipemia (HL)and acute cerebral ischemia/reperfusion (I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase (ALT) and aspartate aminotransferase (AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay.The expression of genes related to apoptosis (caspase-3,bcl-2)was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-α (TNF-α),interleukin-1 (IL-1) and liver mitochondrial superoxide dismutase (SOD),glutathione peroxidase (GSH-Px),malondialdehyde (MDA) and Ca2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1 (CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT (25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels (18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells (4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT (93.62 ± 24.00 vs 9.56± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST (82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells (6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97± 0.47,P < 0.01),elevated expression of caspase-3and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-α,IL-1,liver mitochondrial MDA and Ca2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity (11.76 ± 2.36 vs4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression (3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01)of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to enhanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.

    Does gemcitabine-based combination therapy improve the prognosis of unresectable pancreatic cancer?

    Chen SunDaniel AnsariRoland AnderssonDe-Quan Wu...
    4944-4958页
    查看更多>>摘要:AIM:To assess whether gemcitabine-based combination therapy improves the prognosis of unresectable pancreatic cancer compared with gemcitabine treatment alone.METHODS:A quantitative up-to-date meta-analysis was undertaken to investigate the efficacy of gemcitabine-based combination treatment compared with gemcitabine monotherapy in locally advanced or metastatic pancreatic cancer.Inclusion was limited to highquality randomized clinical trials.RESULTS:Twenty-six studies were included in the present analysis,with a total of 8808 patients recruited.The studies were divided into four subgroups based on the different kinds of cytotoxic agents,including platinum,fluoropyrimidine,camptothecin and targeted agents.Patients treated with gemcitabine monotherapy had significantly lower objective response rate [risk ratio (RR),0.72; 95% confidence interval (CI):0.63-0.83; P < 0.001],and lower 1-year overall survival (RR,0.90; 95%CI:0.82-0.99; P =0.04).Gemcitabine monotherapy caused fewer complications,including fewer grade 3-4 toxicities:including vomiting (RR,0.75; 95%CI:0.62-0.89; P =0.001),diarrhea (RR,0.66; 95%CI:0.49-0.89; P =0.006),neutropenia (RR,0.88; 95%CI:0.72-1.06; P =0.18),anemia (RR,0.96;95%CI:0.82-1.12; P =0.60),and thrombocytopenia (RR,0.76; 95%CI:0.60-0.97; P =0.03) compared with gemcitabine combination therapies.CONCLUSION:Gemcitabine combination therapy provides a modest improvement of survival,but is associated with more toxicity compared with gemcitabine monotherapy.

    Cameron ulcers: An atypical source for a massive upper gastrointestinal bleed

    Samir KapadiaSophia JagroopAtul Kumar
    4959-4961页
    查看更多>>摘要:Cameron lesions represent linear gastric erosions and ulcers on the crests of mucosal folds in the distal neck of a hiatal hernia (HH).Such lesions may be found in upto 50% of endoscopies performed for another indication.Though typically asymptomatic,these may rarely present as acute,severe upper gastrointestinal bleed (GIB).The aim is to report a case of a non-anemic 87-year-old female with history of HH and atrial fibrillation who presented with hematemesis and melena resulting in hypovolemic shock.Repeat esophagogastroduodenoscopy was required to identify multiple Cameron ulcers as the source.Endoscopy in a patient with HH should involve meticulous visualization of hernia neck and surrounding mucosa.Cameron ulcers should be considered in all patients with severe,acute GIB and especially in those with known HH with or without chronic anemia.

    Metastases of esophageal carcinoma to skeletal muscle:Single center experience

    Jan CincibuchMiroslav Myslive(c)ekBohuslav Melichar(C)estmír Neoral...
    4962-4966页
    查看更多>>摘要:Metastases of esophageal carcinoma to the skeletal muscle are rare,but the incidence may be increasing because of better diagnosis resulting from widespread use of positron emission tomography/computed tomography (PET/CT).A cohort of 205 patients with esophageal carcinoma treated at our center who had PET/CT between 2006 and 2010 was retrospectively evaluated for the presence of skeletal muscle metastases.Four patients had skeletal muscle metastases of esophageal carcinoma,including two patients with squamous cell carcinoma.In another patient with squamous cell carcinoma of the esophagus and synchronous skeletal muscle metastases,muscle metastases were subsequently shown to be related to second primary pancreatic adenocarcinoma.In all cases,skeletal muscle metastases were the first manifestation of systemic disease.In three patients palliation was obtained with the combination of external beam radiation therapy,systemic chemotherapy or surgical resection.Skeletal muscle metastases are a rare complication of esophageal carcinoma.

    Hepatic schwannoma: Imaging findings on CT, MRI and contrast-enhanced ultrasonography

    Yu OtaKazunobu AsoKenji WatanabeTakahiro Einama...
    4967-4972页
    查看更多>>摘要:A primary benign schwannoma of the liver is extremely rare and is difficult to preoperatively discriminate from a malignant tumor.We compared the imaging and pathological findings,and examined the possibility of preoperatively diagnosing a benign liver schwannoma.A 72-year-old woman was admitted to our hospital because of a 4.6-cm mass in the liver.A malignant tumor was suspected,and a right hepatectomy was performed.After this,the diagnosis of a primary benign schwannoma of the liver was made through pathological examination.Contrast-enhanced ultrasonography (CEUS) with Sonazoid showed minute blood flows into the septum and solid areas of the tumor in the vascular phase; most likely due to increased arterial flow associated with infiltration of chronic inflammatory cells.In the postvascular phase,CEUS showed contrast defect of cystic areas and delayed enhancement of solid areas; most likely due to aggregation of siderophores.Because discriminating between a benign and malignant schwannoma of the liver is difficult,surgery is generally recommended.However,the two key findings from CEUS may be useful in discriminating ancient schwannoma by recognizing the hemorrhage involved in the secondary degeneration and aggregation of siderophores.

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