Since the discovery of Carnpylobacter-like organisms （Helicobacter pylori） more than two decades ago the possibility of a relationship with gastric cancer has been postulated, tested and supposedly proven. There hav...Since the discovery of Carnpylobacter-like organisms （Helicobacter pylori） more than two decades ago the possibility of a relationship with gastric cancer has been postulated, tested and supposedly proven. There have been numerous human studies of various designs from many countries around the world. Several meta-analyses have been published and more recently a small number of experimental animal studies were reported looking at the association between Helicobacter pylori infection and gastric cancer. Over the years, the human epidemiological studies have produced conflicting results; the metaanalyses have as one would expect produced similar pooled estimates; while the early experimental animal studies require replication. The exact mechanisms by which H pylori might cause gastric cancer are still under investigation and remain to be elucidated.展开更多
Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33...Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33 patients received gastroendoscopy. H.pylori infection was confirmed by Giems staining and bacteria culture under microaerophilic conditions. Expression of iNOS, eNOS and nitrotyrosine were detected by immunohistochemistry. Results: (1) The positive rate of H. pylori infection was 66.7%(22/33). (2) iNOS positive staining in inflammatory cells was detected in 77.3%(17/22) of samples with H.pylori and 27.3%(3/11) without H.pylori infection (P<0.01). (3) eNOS expression in inflammatory cells was found in 77.3%(17/22) of samples with H. pylori and 18.2%(2/11) without H.pylori infection (P<0.01). (4) Nitrotyrosine expression in inflammatory cells was observed in 59.1%(13/22) of samples with H. pylori and 54.5%(6/11) without H. pylori infection (P>0.05). (5) Moderate and severe infiltrations of inflammatory cells were found in 86.4%(19/22) of gastric biopsies with H. pylori and 9.1%(1/11) of samples without H. pylori infection (P<0.01). Conclusion: H.pylori infection might promote infiltration of mononuclear cells and macrophages in gastric mucosa and induce iNOS expression in these cells. The accumulated nitric oxide in local area may result in gastric mucosa damage.展开更多
文摘Since the discovery of Carnpylobacter-like organisms （Helicobacter pylori） more than two decades ago the possibility of a relationship with gastric cancer has been postulated, tested and supposedly proven. There have been numerous human studies of various designs from many countries around the world. Several meta-analyses have been published and more recently a small number of experimental animal studies were reported looking at the association between Helicobacter pylori infection and gastric cancer. Over the years, the human epidemiological studies have produced conflicting results; the metaanalyses have as one would expect produced similar pooled estimates; while the early experimental animal studies require replication. The exact mechanisms by which H pylori might cause gastric cancer are still under investigation and remain to be elucidated.
基金National Natural Science Foundation of China (No.30170427)
文摘Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33 patients received gastroendoscopy. H.pylori infection was confirmed by Giems staining and bacteria culture under microaerophilic conditions. Expression of iNOS, eNOS and nitrotyrosine were detected by immunohistochemistry. Results: (1) The positive rate of H. pylori infection was 66.7%(22/33). (2) iNOS positive staining in inflammatory cells was detected in 77.3%(17/22) of samples with H.pylori and 27.3%(3/11) without H.pylori infection (P<0.01). (3) eNOS expression in inflammatory cells was found in 77.3%(17/22) of samples with H. pylori and 18.2%(2/11) without H.pylori infection (P<0.01). (4) Nitrotyrosine expression in inflammatory cells was observed in 59.1%(13/22) of samples with H. pylori and 54.5%(6/11) without H. pylori infection (P>0.05). (5) Moderate and severe infiltrations of inflammatory cells were found in 86.4%(19/22) of gastric biopsies with H. pylori and 9.1%(1/11) of samples without H. pylori infection (P<0.01). Conclusion: H.pylori infection might promote infiltration of mononuclear cells and macrophages in gastric mucosa and induce iNOS expression in these cells. The accumulated nitric oxide in local area may result in gastric mucosa damage.
