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| 1 | Protective effect of glutamine on intestinal injury and bacterial community in rats exposed to hypobaric hypoxia environment显示文摘AIM:To investigate the protective effect of glutamine(Gln)on intestinal injury and the bacterial community in rats exposed to hypobaric hypoxia environment.METHODS:Sprague-Dawley rats were divided into control,hypobaric hypoxia(HH),and hypobaric hypoxia+Gln(5.0 g/kg BW·d)(HG)groups.On the first 3 d,all rats were placed in a normal environment.After the third day,the HH and HG groups were transferred into a hypobaric chamber at a simulated elevation of 7000m for 5 d.The rats in the HG group were given Gln by gavage daily for 8 d.The rats in the control and HH groups were treated with the same volume of saline.The intestinal morphology,serum levels of malondialdehyde(MDA),superoxide dismutase(SOD),interleukin-6 (IL-6),tumor necrosis factor-α(TNF-α),interferon-gamma(IFN-γ)and diamino oxidase(DAO)were examined.We also evaluated the expression levels of occludin,toll-like receptor 4(TLR4),nuclear factor-κB p65(NF-κB p65)and myeloid differentiation factor 88(MyD88),and examined the bacterial community in caecal contents.RESULTS:Hypobaric hypoxia induced the enlargement of the heart,liver,lung and kidney,and caused spleen atrophy.Intestinal villi damage was also observed in the HH group.Supplementation with Gln significantly alleviated hypobaric-induced damage to main organs including the intestine,increased serum SOD(1.14±0.03 vs 0.88±0.04,P<0.05)and MDA(8.35±1.60,P<0.01)levels and decreased serum IL-6(1172.13±30.49 vs 1407.05±34.36,P<0.05),TNF-α(77.46±0.78 vs 123.70±3.03,P<0.001),IFN-γ(1355.42±72.80 vs 1830.16±42.07,P<0.01)and DAO(629.30±9.15 vs 524.10±13.34,P<0.001)levels.Moreover,Gln significantly increased occludin(0.72±0.05 vs 0.09±0.01,P<0.001),TLR4(0.15±0.05 vs 0.30±0.09,P<0.05),MyD88(0.32±0.08 vs 0.71±0.06,P<0.01),and NF-κB p65(0.16±0.04 vs 0.44±0.03,P<0.01)expression levels and improved the intestinal bacterial community.CONCLUSION:Gln treatment protects from intestinal injury and regulates the gut flora imbalance in hypoxia environment.These effects may be related to the TLR4/MyD88/NF-κB signaling pathway. | Chun-Lan Xu Rui Sun Xiang-Jin Qiao Cui-Cui Xu Xiao-Ya Shang Wei-Ning Niu | 2014 | World Journal of Gastroenterology2014，20，16： | 29 |
| 2 | Morphological study on colonic pathology in ulcerative colitis treated by moxibustion显示文摘AIM To observe the therapeutic effect ofmoxibustion on ulcerative colitis and itsinfluence on the colonic mucosal morphology.METHODS Forty-six patients with ulcerativecolitis were randomly divided into themoxibustion with herbal medicine underneathgroup and the western medicine group.Thirtypatients were treated with the abovemoxibustion and 16 patients with Salicylayefapyridine(SASP).The colonic mucosa of 13patients in the moxibustion group was observedby colonoscopy before and after the treatment.Mucin was also analyzed by H.E and AB-PASstaining.RESULTS Seventeen patients were clinicallycured,12 were improved and 1 unchanged in themoxibustion group.In the control group,5patients were clinically cured,7 improved and 4unchanged.Thirteen patients with active UCwere taken as the subjects for histopathologicanalysis in this study.The colonic mucosallesions were remarkably improved and thecharacteristic of the mucin also changed.Inmost sections,the chronic inflammation ofmucosa was geatly ameliorated(P<0.01).Theinflammatory cell infiltratation much decreased and neutrophils,disapeared in most sections(P<0.001).The goblet cells significantlyincreased(P<0.001);crypt paracrypt abscessor mucosal ulceration was seen(P<0.001).CONCLUSION The rate of cure of ulcerative colitis by moxibustion with herbal medicine beneath is superior to that by SASP. This sort of moxibustion can effectively improve the colonic mucosal lesions and restore the proportion of mucoprotein to near normal. | Huan Gan Wu Li Bin Zhou Da Ren Shi Shi Min Liu Hui Rong Liu Bi Meng Zhang Han Ping Chen Lin Shan Zhang | 2000 | World Journal of Gastroenterology2000，6，6： | 28 |
| 3 | 中医药治疗幽门螺杆菌感染研究进展显示文摘自1982年幽门螺杆菌(Helicobacter pylori,Hp)首次从人胃黏膜组织中分离培养出以来,国内外学者对其进行了30多年的研究,现已证实Hp感染是慢性活动性胃炎、消化性溃疡、胃黏膜相关淋巴组织(mucosa-associated lymphoid tissue,MALT)淋巴瘤和胃癌的主要致病因素。全球有超过50%的人感染有Hp,西方国家感染率为25%-50%。 | 史彬 刘楠洋 毕红岩 唐旭东 李振华 | 2017 | 中国中西医结合杂志2017，37，4： | 27 |
| 4 | Immunocytochemical identification and localization of APUD cells in the gut of seven stomachless teleost fishes显示文摘AIM To study the cell types,localization,distribution density and morphology of APUDcells in the intestinal mucosa of stomachlessteleost fishes.METHOD By using the peroxidase-antiperoxidase complex(PAP)immunocytochemical staining technique theidentification,localization and morphology ofimmunoreactive(IR)endocrine cells seattered inthe intestinal mucosa of grass carp(Cyenopharyngodon idellus),black carp(Mylopharyngodon piceus)and common carp(Cyprinus carpio)were investigated with 20kinds of antisera prepared against mammalianpeptide hormones of APUD cells,and likewise byusing avidin-biotin-peroxidase complex(ABC)method those of silver carp(Hypophthalmichthys molitrix),bighead(Aristichthys nobilis),silver crucian carp(Carassius gibelio)and bluntnose black bream(Megalobrama amblyocephala)were alsostudied with 5 different antisera.Thereplacement of the first antiserum by phosphatebuffered saline(PBS)was employed as a control.IR endocrine cells were counted with asquare-mesh ocular micrometer from 10 fieldsselected randomly in every section of each partof the intestine specimen.The average numberof IR endocrine cells per mm2 was counted toquantify their distribution density.RESULT Gastrin(GAS)-,Gastric inhibitorypeptide(GIP)-,glucagon(GLU)-,glucagon-likeimmunoreactants(GLI)-,bovine pancreaticpolypeptide(BPP)-,leucine-enkephalin(ENK)-and substance P(SP)-IR endocrine cells werefound in the gut of grass carp,black carp andcommon carp,and somatostatin(SOM)-IRendocrine cells were only seen in common carp.GAS-,GIP-and GLU-IR endocrine cells werefound in the intestinal mucosa of silver carp,bighead,silver crucian carp and bluntnose blackbream.Most of IR endocrine cells had the higherdistribution density in the foregut and midgut,and were longer in shape.They had a long apicalcytoplasmic process extended to the gut lumenand a basal process extended to adjacent cellsor basement membrane and touched with it.Sometimes,the basal cytoplasmic processformed an enlarged synapse-like structure in thecontiguous part with basement membrane.Thisphenomenon provided new morphologicalevidence for neuroendocrine and paracrinesecretory function of these enteroendocrinecells.CONCLUTION At least 8 kinds of IR endocrinecells were found in the gut of stomachlessteleost species for the first time in China.TheseIR endocrine cells scattering in the gut mucosabelong to the APUD system.Among them,thehormones secreted by SP-,ENK-,SOM-and GLU-IR endocrine cells belong to the peptides of dualdistribution in the brain and gut.This providednew evidence for the concept of brain-gutpeptide.According to the cell types,distribution density,morphologicalcharacteristics and variety in shape of APUDcells in the gut of stomachless teleost fishes,itis deemed that the digestive tract of fishes isalso an endocrine organ of great importance andcomplexity. | Pan QS Fang ZP Zhao YX | 2000 | World Journal of Gastroenterology2000，6，1： | 25 |
| 5 | Bone-marrow mesenchymal stem cells reduce rat intestinal ischemia-reperfusion injury, ZO-1 downregulation and tight junction disruption via a TNF-α-regulated mechanism显示文摘AIM: To investigate the effect of bone-marrow mesenchymal stem cells (BM MSCs) on the intestinal mucosa barrier in ischemia/reperfusion (I/R) injury. METHODS: BM MSCs were isolated from male Sprague-Dawley rats by density gradient centrifugation, cultured, and analyzed by flow cytometry. I/R injury was induced by occlusion of the superior mesenteric artery for 30 min. Rats were treated with saline, BM MSCs (via intramucosal injection) or tumor necrosis factor (TNF)-α blocking antibodies (via the tail vein). I/R injury was assessed using transmission electron microscopy, hematoxylin and eosin (HE) staining, immunohistochemistry, western blotting and enzyme linked immunosorbent assay.RESULTS: Intestinal permeability increased, tight junctions (TJs) were disrupted, and zona occludens 1 (ZO-1) was downregulated after I/R injury. BM MSCs reduced intestinal mucosal barrier destruction, ZO-1 downregulation, and TJ disruption. The morphological abnormalities after intestinal I/R injury positively correlated with serum TNF-α levels. Administration of anti-TNF-α IgG or anti-TNF-α receptor 1 antibodies attenuated the intestinal ultrastructural changes, ZO-1 downregulation, and TJ disruption. CONCLUSION: Altered serum TNF-α levels play an important role in the ability of BM MSCs to protect against intestinal I/R injury. | Zhong-Yang Shen Jing Zhang Hong-Li Song Wei-Ping Zheng | 2013 | World Journal of Gastroenterology2013，19，23： | 23 |
| 6 | Endoscopic submucosal dissection vs endoscopic mucosal resection for colorectal tumors: A meta-analysis显示文摘AIM: To compare the efficacy and safety of endoscopic submucosal dissection(ESD) and endoscopic mucosal resection(EMR) for the treatment of colorectal tumors.METHODS: Databases, such as PubMed, EMBASE, Cochrane Library and Science Citation Index updated to 2013 were searched to include eligible articles. In the meta-analysis, the main outcome measurements were the en bloc resection rate, the histological resection rate and the local recurrence rate. Meanwhile, we also compared the operation time and the incidence of procedure-related complications.RESULTS: Six trials were identified and a total of 1642 lesions were included. The en bloc resection rate was higher and the local recurrence rate was lower in the ESD group compared with the EMR group(OR = 7.94; 95%CI: 3.96-15.91; OR = 0.09; 95%CI: 0.04-0.19). There was no significant difference in histological resection rate(OR = 1.65; 95%CI: 0.29-9.30) and procedure-related complication rate between the two groups(OR = 1.59; 95%CI: 0.92-2.73). The meta-analysis also showed that ESD was more time consuming than EMR.CONCLUSION: Compared with EMR, ESD results in higher en bloc resection rate and lower local recurrence rate for the treatment of colorectal tumors, without increasing the procedure-related complications. | Jing Wang Xiao-Hua Zhang Jian Ge Chong-Mei Yang Ji-Yong Liu Shu-Lei Zhao | 2014 | World Journal of Gastroenterology2014，20，25： | 21 |
| 7 | Cytomegalovirus and ulcerative colitis:Place of antiviraltherapy显示文摘The link between cytomegalovirus(CMV) infection and inflammatory bowel diseases remains an important subject of debate. CMV infection is frequent in ulcerative colitis(UC) and has been shown to be potentially harmful. CMV reactivation needs to be diagnosed using methods that include in situ detection of viral markers by immunohistochemistry or by nucleic acid amplification techniques. Determination of the density of infection using quantitative tools(numbers of infected cells or copies of the genome) is particularly important. Although CMV reactivation can be considered as an innocent bystander in active flareups of refractory UC, an increasing number of studies suggest a deleterious role of CMV in this situation. The presence of colonic CMV infection is possibly linked to a decreased response to steroids and other immunosuppressive agents. Some treatments, notably steroids and cyclosporine A, have been shown to favor CMV reactivation, which seems not to be the case for therapies using anti-tumor necrosis factor drugs. According to these findings, in flare-ups of refractory UC, it is now recommended to look for the presence of CMV reactivation by using quantitative tools in colonic biopsies and to treat them with ganciclovir in cases of high viral load or severe disease. | Sylvie Pillet Bruno Pozzetto Xavier Roblin | 2016 | World Journal of Gastroenterology2016，22，6： | 19 |
| 8 | Increased susceptibility of aging gastric mucosa to injury:The mechanisms and clinical implications显示文摘This review updates the current views on aging gastric mucosa and the mechanisms of its increased susceptibility to injury.Experimental and clinical studies indicate that gastric mucosa of aging individuals-'aging gastropathy'-has prominent structural and functional abnormalities vs young gastric mucosa.Some of these abnormalities include a partial atrophy of gastric glands,impaired mucosal defense(reduced bicarbonate and prostaglandin generation,decreased sensory innervation),increased susceptibility to injury by a variety of damaging agents such as ethanol,aspirin and other non-steroidal anti-inflammatory drugs(NSAIDs),impaired healing of injury and reduced therapeutic efficacy of ulcer-healing drugs.Detailed analysis of the above changes indicates that the following events occur in aging gastric mucosa:reduced mucosal blood flow and impaired oxygen delivery cause hypoxia,which leads to activation of the early growth response-1(egr-1)transcription factor.Activation of egr-1,in turn,upregulates the dual specificity phosphatase,phosphatase and tensin homologue deleted on chromosome ten(PTEN)resulting in activation of pro-apoptotic caspase-3 and caspase-9 and reduced expression of the anti-apoptosis protein,survivin.The imbalance between pro-and anti-apoptosis mediators results in increased apoptosis and increased susceptibility to injury.This paradigm has human relevance since increased expression of PTEN and reduced expression of survivin were demonstrated in gastric mucosa of aging individuals.Other potential mechanisms operating in aging gastric mucosa include reduced telomerase activity,increase in replicative cellular senescence,and reduced expression of vascular endothelial growth factor and importin-α-a nuclear transport protein essential for transport of transcription factors to nucleus.Aging gastropathy is an important and clinically relevant issue because of:(1)an aging world population due to prolonged life span;(2)older patients have much greater risk of gastroduodenal ulcers and gastrointestinal complications(e.g.,NSAIDs-induced gastric injury)than younger patients;and(3)increased susceptibility of aging gastric mucosa to injury can be potentially reduced or reversed pharmacologically. | Andrzej S Tarnawski Amrita Ahluwalia Michael K Jones | 2014 | World Journal of Gastroenterology2014，20，16： | 16 |
| 9 | Methylation status of p16 gene in colorectal carcinoma and normal colonic mucosa显示文摘 | Zhang J Lai MD Chen J | 1999 | World Journal of Gastroenterology1999，5，5： | 15 |
| 10 | Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition显示文摘BACKGROUND:Emodin,a traditional Chinese medicine,has a therapeutic effect on severe acute pancreatitis(SAP),whereas the underlying mechanism is still unclear.Studies showed that the intestinal mucosa impairment,and subsequent release of endotoxin and proinflammatory cytokines such as IL-1β,which further leads to the dysfunction of multiple organs,is the potentially lethal mechanism of SAP.Caspase-1,an IL-1β-converting enzyme,plays an important role in this cytokine cascade process.Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP.METHODS:Eighty Sprague-Dawley rats were randomly divided into four groups(n=20 each group):SAP,sham-operated(SO),emodin-treated(EM) and caspase-1 inhibitor-treated(ICE-I) groups.SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct.Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction.Serum levels of IL-1β,IL-18 and endotoxin,histopathological alteration of pancreas tissues,intestinal mucosa,and the intestinal caspase-1 m RNA and protein expressions were assessed 24 hours after SAP induction.RESULTS:Rats in the SAP group had higher serum levels of IL-1β and IL-18(P<0.05),pancreatic and gut pathological scores(P<0.05),and caspase-1 m RNA and protein expressions(P<0.05) compared with the SO group.Compared with the SAP group,rats in the EM and ICE-I groups had lower IL-1β and IL-18 levels(P<0.05),lower pancreatic and gut pathological scores(P<0.05),and decreased expression of intestine caspase-1 m RNA(P<0.05).Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions,more disappeared intercellular joints,and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups.CONCLUSIONS:Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP.Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines,including IL-1β and IL-18.Our animal data may be applicable in clinical practice. | Jian-Wen Ning Yan Zhang Mo-Sang Yu Meng-Li Gu Jia Xu Ali Usman Feng Ji | 2017 | Hepatobiliary & Pancreatic Diseases International2017，16，4： | 15 |
| 11 | Effect of bowel rehabilitative therapy on structural adaptation of remnant small intestine: animal experiment显示文摘AIM To investigate the individual and thecombined effects of glutamine, dietary fiber,and growth hormone on the structural adaptationof the remnant small bowel.METHODS Forty-two adult male Sprague-Dawley rats underwent 85% mid-small bowel( TPN ) support during the first threepostoperational days. From the 4thpostoperational day, animals were randomlyassigned to receive 7 different treatments for 8days: TPNcon group, receiving TPN and enteral20 g.L- 1 glycine perfusion; TPN + Gin group,receiving TPN and enteral 20 g.L-1 glutamineperfusion; ENcon group, receiving enteralnutrition (EN) fortified with 20 g@L-1 glycine; EN+ Gin group, enteral nutrition fortified with20g. L-1 glutamine; EN + Fib group, enteralnutrition and 2 g. d- 1 oral soybean fiber; EN + GHgroup, enteral nutrition and subcutaneousgrowth hormone (GH) (0.31U) injection twicedaily; and ENint group, glutamine-enriched EN.oral soybean fiber, and subcutaneous GHinjection.RESULTS Enteral glutamine perfusion duringTPN increased the small intestinal villus height(jejunal villus height 250 μm ±29 μm in TPNconvs 330 μm ± 54 μm in TPN + Gin, ileal villus height260μm±28μm in TPNcon vs 330 μm±22μm inTPN + Gin, P<0.05) and mucosa thickness( jejunal mucosa thickness 360 μm ± 32 μm inTPNcon vs 460 μm ± 65 μm in TPN + Gin, ilealmucosa thickness 400 μm ± 25 μm in TPNcon vs490μm ± 11 μm in TPN + Gin, P<0.05) incomparison with the TPNcon group. Either fibersupplementation or GH administration improvedbody mass gain (end body weight 270 g ± 3.6 g inEN+Fib, 265.7 g ± 3.3 g in EN+GH, vs 257g±3.3g in ENcon, P<0.05), elevated plasmainsulin-like growth factor ( IGF-Ⅰ ) level(880 μg. L-1 ± 52 μg. L-1 in EN + Fib, 1200 μg. L-1± 96 μg. L- 1 in EN ± GH, vs 620 μg. L-1 ±43 μg. L-1 in ENcon, P<0.05), and increased thevillus height (jejunum 560 μm ± 44 μm in EN ± Fib,530 μm± 30 μm in EN ± GH, vs 450 μm ± 44 μm inENcon, ileum 400 μm ± 30 μm in EN + Fib, 380 μm±49 μm in EN± GH, vs 320 μm± 16 μm in ENcon,P<0.05) and the mucosa thickness (jejunum740 μm ± 66 μm in EN ± Fib, 705 μm ± 27 μm in EN ±GH, vs 608 μm ± 58 μm in ENcon, ileum 570 μm ±27 μm in EN ± Fib, 560 μm ± 56 μm in EN ± GH, vs480μm ± 40 μm in ENcon, P<0.05) in remnantjejunum and ileum. Glutamine-enriched ENproduced little effect in body mass, plasma IGF-Ⅰ level, and remnant small bowel mucosalstructure. The ENint group had greater bodymass (280g ± 2.2g), plasma IGF-Ⅰ level(1450g@L-1 ± 137g. L 1), and villus height(jejunum 620 μm ± 56 μm, ileum 450 um ± 31 μm)and mucosal thickness (jejunum 800 μm ± 52 μm,ileum 633 μm± 33 μm) than those in ENcon, EN +Gin (jejunum villus height and mucosa thickness450 μm ± 47 μm and 610 μm ± 63 μm, ileum villusheight and mucosa thickness 330 μm ± 39 μm and500 μm± 52 μm), EN + GH groups (P<0.05), andthan those in EN + Fib group although nostatistical significance was attained.CONCLUSION Both dietary fiber and GH whenused separately can enhance the postresectionalsmall bowel structural adaptation. Simultaneoususe of these two gut-trophic factors can producesynergistic effects on small bowel structuraladaptation. Enteral glutamine perfusion isbeneficial in preserving small bowel mucosalstructure during TPN, but has little beneficialeffect during EN. | Xin Zhou1 Yuan Xin Li2 Ning Li2 Jie Shou Li2 1Department of General Surgery, Medical School, Nanjing University, Nanjing 210093. Jiangsu Province. China2Research Institute of General Hospital. Chinese PLA General Hospital of Nanjing Military Area, Nanjing 210002. Jiangsu Province. China | 2001 | World Journal of Gastroenterology2001，7，1： | 14 |
| 12 | Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa显示文摘AIM To .investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7 d sleep deprivation. RT-PCR,immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70.Ethanol (500 mL@ L 1, I.g.) was used to induce gastric muceea damage.RESULTS RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL@ L-1 ethanol challenge, the ulcer area found in the rats with 7 d sleep deprivation (19.15 ± 4.2) mm2 was significantly lower (P<0.01) than the corresponding control (53.7 ± 8.1) mm2.CONCLUSION Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection. | Xi-Zhong Shen Marcel W.L. Koo Chi-Hin Cho Department of Gastroenterology,Zhongshan Hospital,Fudan University,136 Yixueyuan Road,Shanghai 200032,ChinaDepartment of Pharmacology.Faculty of Medicine,University of Hong Kong,5 Sassoon Road,Pokfulam,Hong Kong,ChinaSupported by .Dr.Marcel W.L.Koo,Department of Pharmacology,FacuLty of Medicine,the University of Hong Kong,5 Sassoon Road,Hong Kong,China.Wlkoo@hkusua.hku.hk | 2001 | World Journal of Gastroenterology2001，7，4： | 14 |
| 13 | Correlations of portal hypertensive gastropathy of hepatitis B cirrhosis with other factors显示文摘Objective: To study the clinical relations of portal hy-pertensive gastropathy (PHG) of hepatitis B cirrho-sis to other factors.Methods: Three groups of subjects were studied pro-spectively at our hospital from March 2000 to March2001: 159 hepatitis B cirrhotic patients with portalhypertension, 114 hepatitis B cirrhotic patients with-out portal hypertension, and 97 control subjects.Free portal vein pressure (FPP) was measured dur-ing surgery. Liver function was assessed by Pugh’smodification of Child’s criteria. The area of livercollagen fibrin was studied using color image analysissystem. Esophageal varices were identified by Dagra-di grading. Gastric varices were identified accordingto Northern Italian Endoscopic Council (NIEC)grading. Hypersplenism was assessed with the reduc-tion of WBC, HGB and PLT. Hepatitis B virus inthe gastric mucosa was detected by immunizing histo-chemistry. Helicobacter pylori (H. pylori) organismswere identified by rapid urease testing and/or exami-nation of the stained biopsy specimens (haematoxylinand eosin). To analyze the correlation between theseendoscopic signs at the gastric level and other fac-tors.Results: The differences of FPP among the threegroups (patients with grade Ⅰ, Ⅱ, and Ⅲ gastropa-thy) were not significant. There was no correlationbetween Child-Pugh classification grading and the se-verity of gastropathy (P=0. 153). The differences ofthe area of liver collagen fibrin among the threegrade gastropathy were not statistically significant (P=0. 801). There was a significant difference in theprevalence of severe PHG among grade Ⅰ, Ⅱ, Ⅲ,Ⅳ and Ⅴ esophageal varices (P<0. 001). PHG waspresent in a similar percentage of patients with gas-tric varices compared with those without gastric vari-ces (P=0. 209). There was a significant difference inthe severity between PHG and hypersplenism (P=0. 003). Seven patients with PHG had no microscopicevidence of hepatitis B virus infection in the gastricwall. There was no correlation between Child-Pughclassification grading and infection of H. pylori (P=0. 7491).Conclusions: The most important element causingPHG is the increased portal pressure as a prerequi-site. In addition, other factors may contribute to thedevelopment of PHG. PHG often occurs in patientswith the presence of esophageal varices. There is amarked correlation between the severity of PHG andhypersplenism. Hepatitis B virus and H. pylori infec-tion are unlikely to be involved in the pathogenesis ofPHG. The development of PHG is less influenced ei-ther by the severity of liver disease (Child-Pughgrade) and cirrhosis or by the presence or non pre-sence of gastric varices. | Wei-Dong Pan Rui-Yun Xun You-Ming Chen the Department of General Surgery Department of Contagious Diseases Third Affiliated Hospital, Zhongshan University, Guangzhou 510630, China | 2002 | Hepatobiliary & Pancreatic Diseases International2002，1，4： | 13 |
| 14 | Endoscopic diagnosis of cervical esophageal heterotopic gastric mucosa with conventional and narrow-band images显示文摘AIM:To compare the diagnostic yield of heterotopic gastric mucosa(HGM)in the cervical esophagus with conventional imaging(CI)and narrow-band imaging(NBI).METHODS:A prospective study with a total of 760patients receiving a CI examination(mean age 51.6years;47.8%male)and 760 patients undergoing NBI examination(mean age 51.2 years;45.9%male).The size of HGM was classified as small(1-5 mm),medium(6-10 mm),or large(>1 cm).A standardized questionnaire was used to obtain demographic characteristics,social habits,and symptoms likely to be related to cervical esophageal HGM,including throat symptoms(globus sensation,hoarseness,sore throat,and cough)and upper esophageal symptoms(dysphagia and odynophagia)at least 3 mo in duration.The clinicopathological classification of cervical esophageal HGM was performed using the proposal by von Rahden et al.RESULTS:Cervical esophageal HGM was found in 36of 760(4.7%)and 63 of 760(8.3%)patients in the CI and NBI groups,respectively(P=0.007).The NBI mode discovered significantly more small-sized HGM than CI(55%vs 17%;P<0.0001).For the 99 patients with cervical esophageal HGM,biopsies were performed in 56 patients;37(66%)had fundic-type gastric mucosa,and 19 had antral-type mucosa.For the clinicopathological classification,77 patients(78%)were classified as HGMⅠ(asymptomatic carriers);21 as HGMⅡ(symptomatic without morphologic changes);and one as HGMⅢ(symptomatic with morphologic change).No intraepithelial neoplasia or adenocarcinoma was found.CONCLUSION:NBI endoscopy detects more cervical esophageal HGM than CI does.Fundic-type gastric mucosa constitutes the most common histology.One-fifth of patients have throat or dysphagic symptoms. | Chi-Liang Cheng Cheng-Hui Lin Nai-Jen Liu Jui-Hsiang Tang Yen-Lin Kuo Yi-Ning Tsui | 2014 | World Journal of Gastroenterology2014，20，1： | 13 |
| 15 | Role of Helicobacter pylori in gastric cancer:Updates显示文摘Helicobacter pylori(H. pylori) infection is highly prevalent in human,affecting nearly half of the world's population; however,infection remains asymptomatic in majority of population. During its co-existence with humans,H. pylori has evolved various strategies to maintain a mild gastritis and limit the immune response of host. On the other side,presence of H.pylori is also associated with increased risk for the development of various gastric pathologies including gastric cancer(GC). A complex combination of host genetics,environmental agents,and bacterial virulence factors are considered to determine the susceptibility as well as the severity of outcome in a subset of individuals. GC is one of the most common cancers and considered as the third most common cause of cancer related death worldwide. Many studies had proved H. pylori as an important risk factor in the development of non-cardia GC. Although both H. pylori infection and GC are showing decreasing trends in the developed world,they still remain a major threat to human population in the developing countries. The current review attempts to highlight recent progress in the field of research on H. pylori induced GC and aims to provide brief insight into H. pylori pathogenesis,the role of major virulence factors of H. pylori that modulates the host environment and transform the normal gastric epithelium to neoplastic one. This review also emphasizes on the mechanistic understanding of how colonization and various virulence attributes of H. pylori as well as the host innate and adaptive immune responses modulate the diverse signaling pathways that leads to different disease outcomes including GC. | Jahanarah Khatoon Ravi Prakash Rai Kashi Nath Prasad | 2016 | World Journal of Gastrointestinal Oncology2016，8，2： | 13 |
| 16 | The Effect of Chinese Tea on Occurrence of Esophageal Tumor Induced by N-Nitrosomethylbenzylamine in Rats显示文摘Five groups of rats (40 rats per group) were given five different varieties of Chinese tea (1 g/50 ml) and another two groups of rats (a positive control and a negative control) were given tap water as drinking water. Except for the negative control group, all the animals were intubated with A’-nitrosomethyibenzylamine (NMBzA, 5 mg/kg body wt/week). Half of the animals in each group were sacrificed after 6 weeks and the remaining animals at the end of 12 weeks. The incidences of esophageal mucosa lesions (16-59%) at the end of6 weeks were significantly lower in the tea-treated rats than in the positive control group (100%). The incidences of esophageal tumor at the end of 12 weeks (42-67%) were also significantly lower in the tea-treated groups than in the positive control group (90%). The same phenomenon was found with respect to the size and number of tumors in each tumor-bearing animal. The relative anticarcinogenic effects of the five varieties of Chinese tea were different. The Fujian oolong tea and jasmine tea exhibited the strongest effects. The results suggest that Chinese tea can effectively inhibit the carcinogenesis Caused by an N-nitroso compound. 1990 Academic Press.Inc. | HI AND XU YONG Institute of Nutrition and Food Hygiene, Chinese Academy of Preventive Medicine, Beijing, China | 1990 | Biomedical and Environmental Sciences1990，3，1： | 11 |
| 17 | Effect of Danshen on apoptosis and NF-кB protein expression of the intestinal mucosa of rats with severe acute pancreatitis or obstructive jaundice显示文摘BACKGROUND:Intestinal mucosa injury in cases of severe acute pancreatitis(SAP) or obstructive jaundice(OJ) is one of the main reasons for the accelerated aggravation of these diseases.Besides being an organ to digest and absorb nutrients,the intestine is also a unique immune organ.When SAP and OJ develop,the destruction of the intestinal mucosa barrier is an important contributing factor for the development of bacterial translocation,systemic inflammatory response syndrome,and multiple organ dysfunction syndrome.It is important to protect the intestinal mucosa in the therapy for SAP and OJ.In this study,we determined the effect of Radix Salviae Miltiorrhizae(Danshen) injection on apoptosis and NF-κB P65 protein expression in the intestinal mucosa of rats with SAP or OJ,and explored the protective mechanism of Danshen in their mucosa.METHODS:Sprague-Dawley rats were used in the SAP and OJ experiments.These rats were randomly divided into shamoperated,model control,and treated groups.At various times after operation,the mortality rates were calculated.Subsequently,the rats were killed to assess the pathological changes,the expression levels of Bax and NF-κB proteins,and the apoptosis indices in the intestinal mucosa.RESULTS:Compared to the corresponding model control group,the number of SAP or OJ rats that died in the treated group decreased but showed no statistically significant difference.At all time points after operation,there was no significant difference between the treated and model control groups in the staining intensity as well as the product of staining intensity and positive staining rate of Bax protein in the intestinal mucosa of SAP and OJ rats.At 3 hours after operation,the apoptosis index of the intestinal mucosa of SAP rats in the treated group was lower than that in the model control group(P<0.01).At 12 hours after operation in SAP rats and 28 days after operation in OJ rats,the staining intensity as well as the product of staining intensity and positive staining rate of NF-κB protein of the intestinal mucosa in the treated group were lower than those in the model control group(P<0.01).CONCLUSION:Danshen exerts protective effects on the intestinal mucosa of SAP and OJ rats perhaps by inhibiting apoptosis and down-regulating NF-κB protein. | | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，5： | 11 |
| 18 | Epidermal growth factor prevents gut atrophy and maintains intestinal integrity in rats with acute pancreatitis显示文摘INTRODUCTIONThere is abundant evidence that stressful insults suchas acute pancreatitis may significantly alter themetabolism of the gut mucosa and therefore itsbarrier integrity,resulting in an increase in mucosalpermeability and subsequent translocation of entericbacteria and their cndotoxins.The fact thatmost bacteria associated with acute pancreatic andperipancreatic infections are of enteric originimplies that the gut plays a major role in | Chen DL Wang WZ Wang JY | 2000 | World Journal of Gastroenterology2000，6，5： | 10 |
| 19 | Study of T-lymphocyte subsets,nitric oxide,hexosamine and Helicobacter pylori infection in patients with chronic gastric diseases显示文摘INTRODUCTIONChronic gastritis(CG)and peptic ulcer(PU)arefrequently-occurring diseases.It is now well recognizedthat Helicobacter pylori(Hp)is a major factor that leadsto CG and PU.In order to study the relationshipamong T lymphocyte subsets,NO,Hexosamine and | Zhang H Jiang SL Yao XX | 2000 | World Journal of Gastroenterology2000，6，4： | 10 |
| 20 | Tumor necrosis factor-α mediates JNK activation response to intestinal ischemia-reperfusion injury显示文摘AIM:To investigate whether tumor necrosis factor-α(TNF-α)mediates ischemia-reperfusion(I/R)-induced intestinal mucosal injury through c-Jun N-terminal kinase(JNK)activation.METHODS:In this study,intestinal I/R was induced by 60-min occlusion of the superior mesenteric artery in rats followed by 60-min reperfusion,and the rats were pretreated with a TNF-α inhibitor,pentoxifylline,or the TNF-α antibody infliximab.After surgery,part of the intestine was collected for histological analysis.The mucosal layer was harvested for RNA and protein extraction,which were used for further real-time polymerase chain reaction,enzyme-linked immunosorbent assay and Western blotting analyses.The TNF-α expression,intestinal mucosal injury,cell apoptosis,activation of apoptotic protein and JNK signaling pathway were analyzed.RESULTS:I/R significantly enhanced expression of mucosal TNF-α at both the mRNA and protein levels,induced severe mucosal injury and cell apoptosis,activated caspase-9/caspase-3,and activated the JNK signaling pathway.Pretreatment with pentoxifylline markedly downregulated TNF-α at both the mRNA and protein levels,whereas infliximab pretreatment did not affect the expression of TNF-α induced by I/R.However,pretreatment with pentoxifylline or infliximab dramatically suppressed I/R-induced mucosal injury and cell apoptosis and significantly inhibited the activation of caspase-9/3 and JNK signaling.CONCLUSION:The results indicate there was a TNFα-mediated JNK activation response to intestinal I/R injury. | Qi Yang Feng-Ping Zheng Ya-Shi Zhan Jin Tao Si-Wei Tan Hui-Ling Liu Bin Wu | 2013 | World Journal of Gastroenterology2013，19，30： | 9 |
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