The issue of drug resistance of Helicobacter pylori is becoming increasingly serious. To analyze the correlation between the cagA and vacA genotypes of H. pylori strains and their resistance to metronidazole, levofloxacin, and clarithromycin in patients in Xi’an, we studied 117 H. pylori strains isolated from patients in Xi’an. Antibiotic susceptibility testing of H. pylori was performed. The cagA and vacA genotypes were investigated using PCR. Among 117 strains of H. pylori, the rate of detection of cagA was 91.45
The present study aimed to elucidate the effect of mast cells (MCs) and eosinophils (Eos) in trinitrobenzenosulphonic acid (TNBS)-induced colitis in SD rats. A rat model of ulcerative colitis (UC) was established by intracolonic injection of 100 mg/kg TNBS (in 0.3 ml 50% ethanol). At 6, 11, 16, 21 days after TNBS injection, the rats were sacrificed to determine the colon injury scores, the counts, distribution, and ultrastructure of mast cells (MCs) and eosinophils (Eos), the concentration of whole blood, and colon histamine. The results showed that after TNBS injection, for 6 days, colon injury score was significantly increased in the distal colon of the rats (P < 0.01 vs. control), accompanied by markedly increased whole blood histamine level and Eos count (P < 0.01), but decreased colon histamine concentration (P < 0.01). At the following 11, 16, 21 days' detection, MCs count and colon histamine level were gradually increased while Eos count and blood histamine were decreased during 21 days' detection period. Furthermore, the correlation analysis revealed that the Eos counts were positively correlated with the colon injury score and blood histamine content (P < 0.05, respectively). The MCs count was negatively associated with the blood histamine content (P < 0.05), but positively associated with the colon tissue histamine content (P < 0.01). In conclusion, though no correlation was found between MCs and Eos counts in the TNBS-induced colitis in this study, their relationship with whole blood and colon histamine appear to play different roles in both the acute and repair stages of colitis.
BXFL (bagasse xylem ferulate)-g-AM (acrylamide)/MAA (methyl methacrylate) was synthesized based on bagasse xylan(BX)-g-AM/MAA in 1-Butyl-3-methylimidazolium chloride ([Bmim] Cl) ion solution with Ferulic Acid (FL) as esterification agent. The various factors that were investigated influenced carboxylic acid ester substitution degree (DSC) of BXFL-g-AM/MAA. The structures of BXFL-g-AM/MAA were confirmed by IR, SEM and 1H NMR analysis. The cytotoxicity of BXFL-g-AM/MAA was investigated against twelve kinds of protein through Surflex-Dock Mode of Sybyl-X 2.0 software, and on three kinds of human cancer cells line and the human normal cells line were detected by MTT assay. It was shown that the maximum DSC was 1.09 in ion solution, which was superior to DSC of conventional method in organic solvent. The results of MTT assay were consistent with docking results. BXFL-g-AM/MAA exhibited relative high cytotoxicity against human gastric cancer cells (MGC-803) line.
Barrett's esophagus (BE) with specialized intestinal metaplasia(SIM) and dysplasia in columnar-lined esophagus (CLE) is difficult to be identified with conventional endoscopy. Narrow band imaging with magnifying endoscopy (NBI-ME) could visualize the subtle superficial mucosal morphology of CLE. In the present study, we assessed the value of mucosal morphology observed by NBI-ME for detection of SIM and dysplasia in CLE. Moreover, the interobserver agreement in the classification of mucosal morphology was been evaluated.
AIM To determine the effects of duodenogastric juice pH on the development of esophageal adenocarcinoma (EAC). METHODS An animal model of duodenogastroesophageal reflux was established using Sprague-Dawley (SD) rats undergoing esophagoduodenostomy (ED). The development of EAC was investigated in rats exposed to duodenogastric juice of different pH. The rats were divided into three groups: low-pH group (group A), high-pH group (group B) and a sham-operated group as a control (group C) (n = 30 rats in each group). The incidence of esophagitis, Barrett's esophagus (BE), intestinal metaplasia with dysplasia and EAC was observed 40 wk after the treatment. RESULTS The incidence rate of esophagitis, BE, intestinal metaplasia with dysplasia and EAC was higher in groups A and B compared with the control group after 40 wk (P < 0.01), being 96% and 100% (P > 0.05), 88% and 82.4% (P > 0.05), 20% and 52.1% (P < 0.05), and 8% and 39% (P < 0.05), respectively. CONCLUSION Non-acidic refluxate increases the occurrence of intestinal metaplasia with dysplasia and EAC while the low-pH gastric juice exerts a protective effect in the presence of duodenal juice. The non-acid reflux is particularly important in the progression from BE to cancer. Therefore, control of duodenal reflux may be an important prophylaxis for EAC.
AIM:To investigate the endoscopy and histology of short-segment Barrett's esophagus (SSBE) and cardia intestinal metaplasia (CIM), and their correlation with Helicobacter pylori (H.pylori ) gastritis and gastroesophageal reflux disease (GERD).METHODS: Biopsy specimens were taken from 32 SSBE patients and 41 CIM patients with normal appearance of the esophagogastric junction.Eight biopsy specimens from the lower esophagus, cardia, and gastric antrum were stained with hematoxylin/eosin, Alcian blue/periodic acid-Schiff, Alcian blue/high iron diamine and Gimenez dye.Results were graded independently by one pathologist. RESULTS:The SSBE patients were younger than the CIM patients (P < 0.01).The incidence of dysplasia and incomplete intestinal metaplasia subtype was higher in SSBE patients than in CIM patients (P < 0.01).H. pylori infection was correlated with antral intestinal metaplasia (P < 0.05), but not with reflux symptomatic, endoscopic, or histological markers of GERD in CIM patients.SSBE was correlated with reflux symptomatic and endoscopic esophagitis (P < 0.01), but not with H. pylori infection and antral intestinal metaplasia.CONCLUSION: Dysplasia risk is significantly greater in SSBE patients than in CIM patients.CIM is a manifestation of H. pylori -associated and multifocal atrophic gastritis, whereas SSBE may result from GERD.
Background: The incidence of esophageal and esophagogastric junction (EGJ) adenocarcinomas is increasing over the last two decades. Barrett's esophagus (BE) is thought to be a premalignant condition of esophageal adenocarcinoma and most of adenocarcinomas at EGJ. Aims: To investigate the expression of Ki-67 in esophagogastric mucosal lesions and its relationship with cell proliferation and apoptosis by tissue microarray. Methods: Using tissue microarray technique, specimens of 140 various esophagogastric mucosal tissues were examined for Ki-67 and proliferating cell nuclear antigen (PCNA) expressions by immunohistochemical method. Cell apoptosis in BE as well as in esophageal and cardiac adenocarcinoma was determined by in situ end-labeling technique (TUNEL method). Results: The positivity rate of Ki-67 in BE, esophageal adenocarcinoma and cardiac adenocarcinoma was 40.9%, 69.6% and 61.9%, respectively, which was significantly higher than that in normal cardiac tissue (0.0%, P<0.01) and cardiac intestinal metaplasia (IM) tissue (11.5%, P<0.05). The positivity rate of PCNA in BE, cardiac IM, antral IM, esophageal adenocarcinoma and cardiac adenocarcinoma was 45.5%, 42.3%, 39.3%, 52.2% and 42.9%, respectively, which was significantly higher than that in normal cardiac tissue (10.0%, P<0.05). In BE, esophageal adenocarcinoma and cardiac adenocarcinoma, the cell apoptotic index in Ki-67 weakly positive and positive tissues was significantly lower than that in Ki-67 negative tissue (P<0.05); while the apoptotic index only in PCNA positive tissue was significantly lower than that in PCNA negative tissue (P<0.05). Conclusions: Abberant Ki-67 expression is involved in the development of BE and adenocarcinoma in EGJ. As compared with PCNA, Ki-67 is a more preferable marker reflecting apoptotic status in EGJ.
目的:研究Ki67和C-erbB-2在各类胃食管黏膜病变中的表达及意义.方法:采用TMA制作140例各类胃食管黏膜病变的组织芯片,分成Barrett食管(BE)组、贲门癌(CA)组、食管腺癌(EA)组、和胃窦肠化(AIM)组、贲门肠上皮化生(CIM)组和正常对照(Control)组,共6组,采用免疫组织化学方法检测Ki67和C-erbB-2的表达.结果:BE组,EA组和CA组Ki67的阳性率均显著高于COntrol组(40.9%,69.6%,61.9% vs 0.0%,均P<0.01),明显高于CIM组11.5%(P<0.05);CIM组和AIM组以及EA组和CA组之间无显著性差异:EA和CA组中Ki67的阳性率高于BE组(P<0.05);BE组,EA组和CA组C-erbB-2的阳性率均显著高于Control组和CIM组(31.8%,52.1%,52.4% vs 0.0%,P<0.01),明显高于AIM组3.6%(P<0.05).C-rbB-2与Ki67在各类胃食管黏膜病变组织中的表达统计学上具有紧密关联性(P=0.001).结论:Ki67和C-erbB-2可能在Barrett食管和胃食管连接处腺癌的发生发展中起重要的促进作用.
BACKGROUND & OBJECTIVE:Intestinal metaplasia (IM) is thought as the precancerous lesion of gastric carcinoma, and CDX2 gene plays important roles in development and differentiation of intestinal epithelium, and maintenance of intestinal phenotype. Recent studies found that CDX2 were expressed aberrantly in IM of chronic atrophic gastritis (CAG) and some gastric carcinomas, which implied that CDX2 may play an important role in IM formation and gastric carcinogenesis. This study was to investigate the roles of CDX2 in the development and progression of IM and gastric carcinogenesis, and determine the correlation of IM to gastric carcinogenesis. METHODS:A tissue microarray containing 46 cases of CAG with IM, 40 cases of gastric carcinoma, and 32 cases of IM foci in paracancerous tissues was constructed. High iron diamine/alcian blue (HID/AB) and HE staining were used to classify IM and gastric carcinoma, and the expression of CDX2 protein and mRNA in different gastric lesions was assessed with immunohistochemistry and in situ hybridization, respectively. RESULTS:The proportion of type III IM was significantly higher in IM foci in paracancerous tissues than in CAG with IM (56.25% vs. 21.74%, P<0.01). The positive rates of CDX2 protein were 69.56% in IM foci in CAG, 53.13% in IM foci in paracancerous tissues, and 42.50% in gastric carcinomas, and the positive rates of CDX2 mRNA were 63.04%, 46.87%, and 35.00%, respectively. The positive rates were significantly lower in gastric cancer than in IM in CAG (P<0.01), but there was no significant difference between gastric cancer and IM foci in paracancerous tissues (P>0.05). The expression of CDX2 protein and mRNA was significantly higher in intestinal-type gastric cancer than in diffuse-type gastric cancer (54.55% vs. 27.78%, 45.45% vs. 22.22%, P<0.05). The expression of CDX2 protein was significantly lower in type III IM than in type I IM (46.42% vs. 79.31%, P<0.05). CONCLUSIONS:CDX2 may play important roles in the development and progression of IM and gastric carcinogenesis.
AIM:To investigate the difference of gene expression profiles between Barrett's esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats. METHODS:Eight-week-old Sprague-Dawley rats were treated esophagoduodenostomy to produce gastroduodenoesophageal reflux, and another group received sham operation as control.Esophageal epithelial tissues were dissected and frozen in liquid nitrogen immediately for pathology 40 wk after surgery.The expression profiles of 4 096 genes in reflux esophagitis and Barrett's esophagus tissues were compared with normal esophageal epithelium by cDNA microarray. RESULTS:Four hundred and forty-eight genes in Barrett's esophagus were more than three times different from those in normal esophageal epithelium, including 312 upregulated and 136 down-regulated genes.Two hundred and thirty-two genes in RE were more than three times different from those in normal esophageal epithelium, 90 up-regulated and 142 down-regulated genes.Compared to reflux esophagitis, there were 214 up-regulated and 142 down-regulated genes in Barrett's esophagus. CONCLUSION:Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux can develop esophagitis and Barrett's esophagus gradually.The gene expression level is different between reflux esophagitis and Barrett's esophagus and the differentially expressed genes might be related to the occurrence and development of Barrett's esophagus and the promotion or progression in adenocarcinoma.
AIM To study the different gene expression profiles in rats with Barrett's esophagus (BE) and esophageal adenocarcinoma (EA) induced by gastro-duodeno-esophageal reflux. METHODS Esophagoduodenostomy was performed in 8-wk old Sprague-Dawley rats to induce gastro-duodeno-esophageal reflux, and a group of rats that received sham operation served as control. Esophageal epithelial pathological tissues were dissected and frozen in liquid nitrogen immediately. The expression profiles of 4096 genes in EA and BE tissues were compared to normal esophagus epithelium in normal control (NC) by cDNA microarray. RESULTS Four hundred and forty-eight genes in BE were more than three times different from those in NC, including 312 upregulated and 136 downregulated genes. Three hundred and seventy-seven genes in EA were more than three times different from those in NC, including 255 upregulated and 142 downregulated genes. Compared to BE, there were 122 upregulated and 156 downregulated genes in EA. In the present study, the interested genes were those involved in carcinogenesis. Among them, the upregulated genes included cathepsin C, aminopeptidase M, arachidonic acid epoxygenase, tryptophan-2,3-dioxygenase, ubiquitin-conjugating enzyme, cyclic GMP-stimulated phosphodiesterase, tissue inhibitor of metalloproteinase-1, betaine-homocysteine methyltransferase, lysozyme, complement 4b binding protein, complement 9 protein, insulin-like growth factor binding protein, UDP-glucuronosyltransferase, tissue inhibitor of metalloproteinase-3, aldolase B, retinoid X receptor gamma, carboxylesterase and testicular cell adhesion molecule 1. The downregulated genes included glutathione synthetase, lecithin-cholesterol acyltransferase, p55CDC, heart fatty acid binding protein, cell adhesion regulator and endothelial cell selectin ligand. CONCLUSION Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux may develop into BE and even EA gradually. The gene expression level is different between EA and BE, and may be related to the occurrence and progression of EA.
AIM:To investigate the roles of mucin histochemistry, cytokeratin 7/20 (CK7/20) immunoreactivity, clinical characteristics and endoscopy to distinguish short-segment Barrett's esophageal (SSBE) from cardiac intestinal metaplasia (CIM).METHODS:High iron diamine/Alcian blue (HID/AB) mucin-histochemical staining and immunohistochemical staining were used to classify intestinal metaplasia (IM) and to determine CK7/20 immunoreactivity pattern in SSBE and CIM, respectively, and these results were compared with endoscopical diagnosis and the positive rate of gastroesophageal reflux disease (GERD) symptoms and H pylori infection. Long-segment Barrett's esophageal and IM of gastric antrum were designed as control.RESULTS:The prevalence of type III IM was significantly higher in SSBE than in CIM (63.33% vs 23.08%, P< 0.005). The CK7/20 immunoreactivity in SSBE showed mainly Barrett's pattern (76.66%), and the GERD symptoms in most cases which showed Barrett's pattern were positive, whereas H pylori infection was negative. However, the CK7/20 immunoreactivity in CIM was gastric pattern preponderantly (61.54%), but there were 23.08% cases that showed Barrett's pattern. H pylori infection in all cases which showed gastric pattern was significantly higher than those which showed Barrett's pattern (63.83% vs 19.30%, P< 0.005), whereas the GERD symptoms in gastric pattern were significantly lower than that in Barrett's pattern (21.28% vs 85.96%, P< 0.005).CONCLUSION:Distinction of SSBE from CIM should not be based on a single method; however, the combination of clinical characteristics, histology, mucin histochemistry, CK7/20 immunoreactivity, and endoscopic biopsy should be applied. Type III IM, presence of GERD symptoms, and Barrett's CK7/20 immunoreactivity pattern may support the diagnosis of SSBE, whereas non-type III IM, positive H pylori infection, and gastric CK7/20 immunoreactivity pattern may imply CIM.
AIM:To assess the diagnostic value of a combination of continuous intragastric pH and bilirubin monitoring in the detection of duodenogastric reflux (DGR), and the effects of diet on the bilirubin absorbance. METHODS:30 healthy volunteers were divided into two groups: standard diet group (Group 1) 18 cases, free diet group (Group 2)12 cases. Each subjects were subjected to simultaneous 24-hour intragastric pH and spectrophotometric bilirubin concentration monitoring (Bilitec 2000). RESULTS:There was no difference of preprandial phase bilirubin absorbance between two groups. The absorbance of postprandial phase was significantly increased in group 2 than group 1. There was no difference between preprandial phase and postprandial phase absorbance in group 1. Postprandial phase absorbance was significantly higher in group 2. In a comparison of bile reflux with intragastric pH during night time, there were 4 types of reflux: Simultaneous increase in absorbance and pH in only 19.6%, increase in bilirubin with unchanged pH 33.3%, pH increase with unchanged absorbance 36.3%, and both unchanged in 10.8%. Linear regression analysis showed no correlation between percentage total time of pH<4 and percentage total time of absorbance>0.14, r=0.068 P<0.05. CONCLUSION:Because of the dietary effect, high absorbance fluids or foods should be avoided in detection. Intragastric pH and bilirubin monitoring separately predict the presence of duodenal (and/or pancreatic) reflux and bile reflux. They can not substitute for each other. The detection of DGR is improved if the two parameters are combined simultaneously.
OBJECTIVE : The aim of the present study was to investigate the factors predisposing patients with Barrett’s esophagus (BE) to intestinal metaplasia (IM). METHODS : Forty‐seven BE patients were studied. By using endoscopic and histological methods, esophageal IM was diagnosed in 36 patients, who were compared with 11 patients without IM in regard to their age, the endoscopic appearance of the esophagus and esophageal motility. RESULTS : The patients’ age and endoscopic features of the esophagus, but not esophageal motor function and grade of macroscopic esophagitis, were risk factors for the development of IM. CONCLUSIONS : Patient age and endoscopic features of the BE mucosa are associated with IM and may be prognostic factors for BE.