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Gastric Tissue (gastric + tissue)
Selected AbstractsEffects of Aspirin on the Development of Helicobacter pylori -Induced Gastric Inflammation and Heterotopic Proliferative Glands in Mongolian GerbilsHELICOBACTER, Issue 1 2008Guo Qing Li Abstract Background: Helicobacter pylori infection is a major cause of gastritis and gastric carcinoma. Aspirin has anti-inflammatory and antineoplastic activity. The aim of the present study was to determine the effects of aspirin on H. pylori -induced gastritis and the development of heterotopic proliferative glands. Methods: H. pylori strain SS1 was inoculated into the stomachs of Mongolian gerbils. Two weeks after inoculation, the animals were fed with the powder diets containing 0 p.p.m. (n = 10), 150 p.p.m. (n = 10), or 500 p.p.m. (n = 10) aspirin. Mongolian gerbils were killed after 36 weeks of infection. Uninfected Mongolian gerbils (n = 10) were used as controls. Histologic changes, epithelial cell proliferation and apoptosis, and prostaglandin E2 (PGE2) levels of gastric tissue were determined. Results: H. pylori infection induced gastric inflammation. Administration of aspirin did not change H. pylori -induced gastritis, but alleviated H. pylori -induced hyperplasia and the development of heterotopic proliferative glands. Administration of aspirin accelerated H. pylori -associated apoptosis but decreased H. pylori -associated cell proliferation. In addition, the increased gastric PGE2 levels due to H. pylori infection were suppressed by treatment with aspirin, especially at the dose of 500 p.p.m. Conclusions: Aspirin alleviates H. pylori -induced hyperplasia and the development of heterotopic proliferative glands. Moreover, aspirin increases H. pylori -induced apoptosis. We demonstrated the antineoplastic activities of aspirin in H. pylori -related gastric carcinogenesis. [source] Quantitative analysis of lymphangiogenic markers for predicting metastasis of human gastric carcinoma to lymph nodesINTERNATIONAL JOURNAL OF CANCER, Issue 3 2005Yasuhiko Kitadai Abstract The spread of tumor cells to regional lymph nodes is an early event of gastric cancer metastasis. In our study, we assessed the expression of lymphangiogenic factors and lymphatic endothelial markers in gastric carcinoma tissues and compared expression levels with the status of lymph node metastasis. We also examined the correlation between lymphatic vessel density (LVD) in primary tumors and lymph node metastasis. Paired biopsy samples (tumor and corresponding normal mucosa) of gastric tissue were obtained from 39 patients with gastric carcinoma. The expression of VEGF-C, VEGF-D, VEGFR-3 and podoplanin mRNAs was assessed by real-time quantitative PCR. The expression of VEGF-C (but not of VEGF-D) was significantly greater in patients with lymph node metastasis than in those without metastasis. The expression of lymphatic endothelial markers VEGFR-3 and podoplanin was also significantly greater in the node-positive group. LVD, as assessed by immunohistochemistry for podoplanin, was correlated with lymph node metastasis. These results indicate that quantitative analysis of lymphangiogenic markers in gastric biopsy specimens may be useful in predicting metastasis of gastric cancer to regional lymph nodes. © 2005 Wiley-Liss, Inc. [source] Autofluorescence imaging analysis of gastric cancerJOURNAL OF DIGESTIVE DISEASES, Issue 3 2002Shu Dong XIAO AIMS: To investigate the characteristics of gastric cancer in autofluorescence images. METHODS: A double-channel laser scanning confocal microscope with an argon ion laser (excitation wavelength 488 nm) and helium,neon laser (excitation wavelength 543 nm) were used to detect autofluorescence from 16 gastric cancer tissue specimens and corresponding normal gastric tissue. RESULTS: Autofluorescence from normal gastric tissue produced a green-colored image. The intensity of red color increased obviously in all gastric cancer tissues (100%) after illumination and the tissues produced a reddish-brown-colored image. CONCLUSIONS: A reddish-brown image is characteristic of autofluorescence in gastric cancer detected by an argon ion laser and helium,neon laser with a double-channel laser scanning confocal microscope. Autofluorescence imaging analysis is useful in the diagnosis of gastric cancer. [source] Expression of COX-1, COX-2 and inducible nitric oxide synthase in superficial gastritis, mucosal dysplasia and gastric carcinomaJOURNAL OF DIGESTIVE DISEASES, Issue 3 2001Yuqin Luo OBJECTIVE: To investigate the significance of the expression of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in superficial gastritis, gastric mucosal dysplasia and gastric carcinoma, and to study the relationship between COX-2, iNOS, gastric carcinoma and Helicobacter pylori infection. METHODS: Polyclonal antibodies to COX-1, COX-2 and iNOS were used detect their expression and the status of H. pylori infection in 92 specimens of paraffin-embedded gastric tissue. Of the 92 patients, 33 had superficial gastritis, 30 had gastric mucosal dysplasia and 29 had gastric cancer. Helicobacter pylori was detected by toluidine blue staining. RESULTS: Expression of COX-2 and iNOS in gastric cancer (65.5%, 62.1%) was significantly higher than that in gastritis (18.2%, 18.2%; P < 0.01). Expression of COX-2 and iNOS in gastritis with H. pylori infection was higher than that in gastric mucosal dysplasia with H. pylori infection. The expression of COX-2 and iNOS occurred concomitantly in gastritis, dysplasia and gastric cancer. CONCLUSION: Inflammation and H. pylori infection may be able to stimulate the expression of COX-2 and iNOS, which might be involved in gastric carcinogenesis. [source] Helicobacter pylori in patients can be killed by visible lightLASERS IN SURGERY AND MEDICINE, Issue 4 2005Robert A. Ganz MD Abstract Background Helicobacter pylori colonizes the mucus layer of the human stomach and may cause peptic ulcer and adenocarcinoma. Novel antimicrobial approaches are sought due to the occurrence of antibiotic resistance and consequent treatment failure. We report here that H. pylori is susceptible to inactivation by blue light. Study Design/Materials and Methods A controlled, prospective, blinded, trial of endoscopically delivered blue light to eradicate H. pylori in regions of the gastric antrum, in 10 patients between the ages of 21 and 80 who tested positive for H. pylori. Light (405 nm) (40 J/cm2) was delivered to a 1-cm diameter spot in the gastric antrum via optical fiber passed through the endoscope and weighed biopsies were taken from treated and control spots and colonies quantitatively cultured. Results Blue light killed 5 logs of bacteria in vitro. The mean reduction in H. pylori colonies per gram tissue between treated and control spots was 91% (7.4±4.8×106 vs. 8.1±1.9×107, two-tailed P<0.0001). Some patients had reductions approaching 99%. No differences were observed on histological examination of light-treated and control gastric tissue. Conclusion Blue light phototherapy may represent a novel approach to eradication of H. pylori, particularly, in patients who have failed standard antibiotic treatment. © 2005 Wiley-Liss, Inc. [source] Pantoprazole, azithromycin and tinidazole: short duration triple therapy for eradication of Helicobacter pylori infectionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2000C. Calabrese Background: Azithromycin is an acid-stable macrolide that achieves remarkably high concentrations in gastric tissue, persisting above the MIC90 for Helicobacter pylori over a period of 5-days, after a single 500 mg oral dose. Aim: To evaluate and compare the efficacy, safety, and tolerability of two eradicating regimens of pantoprazole, azithromycin and tinidazole. Methods: A total of 100 consecutive symptomatic H. pylori- positive patients received pantoprazole 40 mg b.d. for 1 week, and were randomly assigned to either azithromycin 500 mg o.m. and tinidazole 500 mg b.d. during the first 3 days (early group, n=50) or during the last 3 days of therapy with pantoprazole (late group, n=50). H. pylori status was assessed by histology and rapid urease test at entry and by histology and 13C-urea breath test 1 month after the end of the therapy. Results: Ninety-nine patients completed the study. H. pylori was eradicated in 86% of patients in the early group (intention-to-treat 86%) and in 88% of patients in the late group (intention-to-treat 88%). Conclusions: This short triple therapy is effective for H. pylori eradication. The compliance was excellent and side-effects negligible. Moreover, the pantoprazole pre-treatment did not modify the efficacy of the therapy. [source] Long-term infection with Helicobacter felis and inactivation of the tumour suppressor gene p53 cumulatively enhance the gastric mutation frequency in Big Blue® transgenic miceTHE JOURNAL OF PATHOLOGY, Issue 4 2003Peter J Jenks Abstract The aims of this study were to determine whether colonization with Helicobacter felis resulted in the accumulation of mutations within murine gastric tissue and whether the degree of genetic damage was increased by p53 deficiency. Female C57BL/6 mice carrying either the lambda/lacI transgene (Big Blue® transgenic mice) or the lambda/lacI transgene and deficient in one allele of the p53 tumour suppressor gene (TSG-p53®/Big Blue®) were inoculated with H felis. Seven months after inoculation, mutations in the target lacI gene were assessed using the Big Blue® transgenic mutagenesis assay system in these animals and in controls. There was an approximately two-fold increase in lacI mutations in gastric mucosa harvested from mice infected with H felis and also from non-infected mice heterozygous for the p53 allele relative to wild-type mice. The mutation frequency in mice infected with H felis and deficient in one allele of p53 was increased approximately three-fold. Active gastric inflammation was significantly greater in H felis -infected p53 hemizygous mice compared with H felis p53 wild-type mice. Gastric epithelial proliferation was similarly increased with infection in both of these latter groups of mice. In infected mice, there was a significant correlation between the mutation frequency and the degree of active gastric inflammation. These data suggest a synergistic action between infection with H felis and p53 deficiency in the accumulation of mutations within gastric tissue. Active neutrophil infiltration in gastric Helicobacter infection may contribute to the increased levels of mutation observed. Copyright © 2003 John Wiley & Sons, Ltd. [source] Investigation of the Immunomodulatory Effects of Lactobacillus casei and Bifidobacterium lactis on Helicobacter pylori InfectionHELICOBACTER, Issue 3 2008Li Zhang Abstract Background:,Lactobacillus and Bifidobacterium species have shown beneficial effects in the treatment of Helicobacter pylori infection; however, the mechanisms behind such effects are not fully understood. In this study, we have investigated the immunomodulatory effects of probiotics in a mouse model of H. pylori infection. Materials and methods:,H. pylori -infected C57BL/6 mice were treated with L. casei L26, B. lactis B94, or no probiotics for 5 weeks, respectively. Mice not infected with H. pylori were included as normal controls. Gastric histology, protein levels of interleukin (IL)-1,, IL-10, IL-12/23p40, and H. pylori colonization density in the gastric tissues, as well as H. pylori -specific antibodies were examined. Results:, In mice receiving L. casei L26 and B. lactis B94, gastric neutrophil infiltration and IL-1, were significantly decreased and IL-10 was significantly increased as compared with mice receiving no probiotics. In mice receiving B. lactis B94, IL-12/23p40 was significantly increased and H. pylori IgG was significantly reduced as compared with mice receiving no probiotics. No significant difference of H. pylori colonization was observed among the three groups of mice. Conclusion:, The reduced level of IL-1, and neutrophil infiltration observed in mice infected with H. pylori following treatment with L. casei L26 and B. lactis B94 resulted from a modulation of immune response rather than a decrease of H. pylori colonization. Furthermore, B. lactis B94 has the intrinsic ability to promote a Th1 immune response through an increase in IL-12/IL-23. [source] Interleukin-10 expression significantly correlates with minor CD8+ T-cell infiltration and high microvessel density in patients with gastric cancerINTERNATIONAL JOURNAL OF CANCER, Issue 8 2006Teruhisa Sakamoto Abstract We aimed to investigate the relationships between interleukin-10 (IL-10) expression and both the clinicopathological findings and prognoses in patients with gastric cancer and to compare IL-10 expression with microvessel (MV) density and CD8+ T lymphocyte infiltration to evaluate its effects on angiogenesis and immune responses in gastric cancer. IL-10 expression was determined in gastric cancer patients by reverse transcription-polymerase chain reaction (RT-PCR) or immunohistochemical procedures. Two of 7 normal gastric tissues showed IL-10 mRNA expression, while its expressions were confirmed in all advanced gastric carcinoma tissues examined (n = 11) by RT-PCR. Immunohistochemical staining demonstrated that IL-10 expression was detected in 52 (47.7%) of 109 cases. There was a close correlation between IL-10 expression and MV density. IL-10 expression inversely correlated with CD8+ T-lymphocyte infiltration. The prognoses of patients whose tumors expressed IL-10 were significantly worse than those of patients whose tumors did not express IL-10. Multivariate analysis indicated IL-10 expression was an independent prognostic factor. IL-10 might be associated with tumor progression by stimulating angiogenesis and suppressing immune responses in gastric cancer. © 2005 Wiley-Liss, Inc. [source] Gastroprotective properties of Myristica malabarica against indometacin-induced stomach ulceration: a mechanistic explorationJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2007Debashish Banerjee The healing activity of the methanol extract of the spice rampatri, Myristica malabarica, (RM) and omeprazole against indometacin-induced stomach ulceration has been studied in a mouse model. Treatment with RM (40 mg kg,1 per day) and omeprazole (3 mg kg,1 per day) for 3 days could effectively heal the stomach ulceration, as revealed from the ulcer indices and histopathological studies. Compared with the ulcerated group, treatment with RM and omeprazole for 3 days reduced the macroscopic damage score by approximately 72% and 76%, respectively (P < 0.001), establishing the efficacy of RM. The extent of ulcer healing offered by 3 days' treatment with RM or omeprazole was better than that observed with natural recovery over 5 and 7 days (P < 0.05). The healing capacities of RM and omeprazole could be attributed to their antioxidant activity as well as the ability to enhance the mucin content of the gastric tissues. Both drugs reduced lipid peroxidation (by 42,44%) and protein carbonyl content (by 34%), and augmented non-protein thiol levels beyond normal values. Furthermore, RM improved the mucin level beyond the normal value, while omeprazole restored it to near normalcy. [source] Synaptic specializations exist between enteric motor nerves and interstitial cells of Cajal in the murine stomachTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2005Elizabeth A.H. Beckett Abstract Autonomic neurotransmission is thought to occur via a loose association between nerve varicosities and smooth muscle cells. In the gastrointestinal tract ultrastructural studies have demonstrated close apposition between enteric nerves and intramuscular interstitial cells of Cajal (ICC-IM) in the stomach and colon and ICC in the deep muscular plexus (ICC-DMP) of the small intestine. In the absence of ICC-IM, postjunctional neural responses are compromised. Although membrane specializations between nerves and ICC-IM have been reported, the molecular identity of these specializations has not been studied. Here we have characterized the expression and distribution of synapse-associated proteins between nerve terminals and ICC-IM in the murine stomach. Transcripts for the presynaptic proteins synaptotagmin, syntaxin, and SNAP-25 were detected. Synaptotagmin and SNAP-25-immunopositive nerve varicosities were concentrated in varicose regions of motor nerves and were closely apposed to ICC-IM but not smooth muscle. W/WV mice were used to examine the expression and distribution of synaptic proteins in the absence of ICC-IM. Transcripts encoding synaptotagmin, syntaxin, and SNAP-25 were detected in W/WV tissues. In the absence of ICC-IM, synaptotagmin and SNAP-25 were localized to nerve varicosities. Reverse transcriptase polymer chain reaction (RT-PCR) and immunohistochemistry demonstrated the expression of postsynaptic density proteins PSD-93 and PSD-95 in the stomach and expression levels of PSD-93 and PSD-95 were reduced in W/WV mutants. These data support the existence of synaptic specializations between enteric nerves and ICC-IM in gastric tissues. In the absence of ICC-IM, components of the synaptic vesicle docking and fusion machinery is trafficked and concentrated in enteric nerve terminals. J. Comp. Neurol. 493:193,206, 2005. © 2005 Wiley-Liss, Inc. [source] Enhancer of zeste homolog 2 expression is associated with tumor cell proliferation and metastasis in gastric cancerAPMIS, Issue 3 2010JUNG HYE CHOI Choi JH, Song YS, Yoon JS, Song KW, Lee YY. Enhancer of zeste homolog 2 expression is associated with tumor cell proliferation and metastasis in gastric cancer. APMIS 2010; 118: 196,202. The enhancer of zeste homolog 2 (EZH2), a member of the polycomb group of proteins, plays an important role in cell proliferation and cell cycle regulation. EZH2 is overexpressed in aggressive forms of prostate, breast, bladder, and endometrial cancers. However, the role of EZH2 expression in gastric cancer has not been fully determined. This study was conducted to investigate the correlation between EZH2 and cell cycle-related molecules, and the clinical value of EZH2 expression in gastric cancer. We analyzed EZH2 expression using Western blotting in AGS, MKN-28, SNU-16, SNU-484, SNU-601, and SNU-638 gastric cancer cell lines. After transfection of EZH2 siRNA into MKN-28 cells, the change in cell cycle-related molecules was assessed by Western blot analysis. Expression of EZH2, Ki-67, and p53 was determined by immunohistochemical staining of tissue microarrays from specimens of 137 cases of resected gastric cancer. We found high expressions of EZH2 in all of the tested gastric cancer cell lines. RNA interference of EZH2 induced upregulation of p53 and HDAC1 and downregulation of cyclin D1 and cyclin E. High EZH2 expression was observed in 60.6% of gastric cancers and in 6.7% of non-neoplastic gastric tissues (p < 0.01); 40.1% were positive for p53 in gastric cancers. High EZH2 expression was correlated with Ki-67 and p53 expressions and was significantly associated with distant metastases and non-signet ring cells. Our results suggest that high EZH2 expression is associated with tumor cell proliferation and metastasis in gastric cancer. [source] Expression of seven gastric cancer-associated genes and its relevance for Wnt, NF-,B and Stat3 signaling,APMIS, Issue 12 2007JING-CHUN HAN The aim of the current study was to profile c-Myc, standard CD44 (CD44s), CD44v6, cyclin D1, survivin, MMP-7 and VEGF expression patterns in different gastric samples and to elucidate their relevance for Wnt, NF-,B and/or Stat3 activation using multiple experimental approaches. The results revealed that 87.1% (27/31) of gastric cancers and 8.7% (2/23) of noncancerous lesions (chronic gastritis and intestinal metaplasia) showed Wnt activation (Wnt+) that was closely related to the expression of the seven genes. Some Wnt, noncancerous lesions also expressed the above-mentioned genes, higher frequencies of survivin (7/8), VEGF (7/8), cyclin D1 (6/8) and c-Myc (5/8) but not CD44s (2/8), CD44v6 (3/8) and MMP-7 (2/8) being detected in the NF-,B+ samples. Stat3 was activated in 37/54 gastric tissues, and in 3/4 VEGF, 4/6 c-Myc, 4/8 survivin, 2/4 MMP-7, 1/2 CD44v6, and 4/9 cyclin D1+ but Wnt,/NF-,B, samples. These findings showed a close correlation in GCs between Wnt, NF-,B and Stat3 signaling and expression of the seven genes, the importance of NF-,B and Stat3 activation in regulating c-Myc, survivin, cyclin D1 and VEGF in noncancerous lesions, and the potential coordinative effects of these three signalings on GC formation presumably by promoting the transcription of their common target genes. [source] Hypermethylation of the TSLC1 Gene Promoter in Primary Gastric Cancers and Gastric Cancer Cell LinesCANCER SCIENCE, Issue 8 2002Teiichiro Honda The TSLC1 (tumor suppressor in lung cancer,1) gene is a novel tumor suppressor gene on chromosomal region 11q23.2, and is frequently inactivated by concordant promoter hypermethylation and loss of heterozygosity (LOH) in non-small cell lung cancer (NSCLC). Because LOH on 11q has also been observed frequently in other human neoplasms including gastric cancer, we investigated the promoter methylation status of TSLC1 in 10 gastric cancer cell lines and 97 primary gastric cancers, as well as the corresponding non-cancerous gastric tissues, by bisulfite-SSCP analysis followed by direct sequencing. Allelic status of the TSLC1 gene was also investigated in these cell lines and primary gastric cancers. The TSLC1 promoter was methylated in two gastric cancer cell lines, KATO-III and ECC10, and in 15 out of 97 (16%) primary gastric cancers. It was not methylated in non-cancerous gastric tissues, suggesting that this hypermethylation is a cancer-specific alteration. KATO-III and ECC10 cells retained two alleles of TSLC1, both of which showed hypermethylation, associated with complete loss of gene expression. Most of the primary gastric cancers with promoter methylation also retained heterozygosity at the TSLC1 locus on 11q23.2. These data indicate that bi-allelic hypermethylation of the TSLC1 promoter and resulting gene silencing occur in a subset of primary gastric cancers. [source] MELATONIN PROTECTS AGAINST HYDROGEN PEROXIDE-INDUCED GASTRIC INJURY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2009Ahmed M Mohamadin SUMMARY 1Melatonin (MT) is a pineal hormone that is also abundant in the gut and has a well known role in scavenging oxygen free radicals. The aim of the present study was to evaluate the potential protective effects of MT against H2O2 -induced gastric lesions in rats. 2An experimental model of gastric ulceration was established in rats using 15% H2O2. Melatonin (12.5, 25 or 50 mg/kg, intagastrically) was administered to rats 30 min before H2O2 challenge. 3Intragastric administration of H2O2 resulted in haemorrhagic lesions in the fundic area of the stomach. Furthermore, H2O2 induced gastric oxidative stress, as indicated by depletion of reduced glutathione (GSH), inhibition of glutathione peroxidase (GPx) activity and elevation of malonedialdehyde (MDA) levels. These effects were accompanied by decreased gastric tissue levels of prostaglandin (PG) E2 and nitric oxide (NO), as well as increased levels of tumour necrosis factor (TNF)-,. Administration of MT (12.5, 25 or 50 mg/kg) 30 min before H2O2 significantly attenuated the development of gastric lesions in a dose-dependent manner. The protective effects of MT were accompanied by significant inhibition of the H2O2 -induced reduction in gastric content of GSH and GPx activity and elevation in MDA levels. Furthermore, MT antagonized H2O2 -induced reduction of gastric PGE2 and NO levels and elevation of TNF-,. 4In conclusion, MT protects rat gastric mucosa against H2O2 -induced damage. The observed protective effects of MT can be attributed, at least in part, to its anti-oxidant properties, preservation of PGE2 and NO levels, as well as inhibition of TNF-, induction in gastric tissues. [source] | |||||||||||||||||||