AIM： To investigate the occurrence of chromosome 3, 7, 8, 9, and 17 aneuploidies, TPS3 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H...AIM： To investigate the occurrence of chromosome 3, 7, 8, 9, and 17 aneuploidies, TPS3 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H pylori infection. METHODS： Gastric biopsies from normal mucosa （NM, n = 10）, chronic gastritis （CG, n = 38）, atrophic gastritis （CAG, n=13） and gastric ulcer （GU, n=21） were studied using fluorescence in situ hybridization （FISH） and immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect Hpylori. An association of the gastric pathologies and aneuploidies with Hpylori infection was assessed. RESULTS： Aneuploidies were increasingly found from CG （21%） to CAG （31%） and to GU （62%）, involving mainly monosomy and trisomy 7, trisomies 7 and 8, and trisomies 7, 8 and 17, respectively. A significant association was found between H pylori infection and aneuploidies in CAG （P=0.0143） and GU （P=0.0498）. No TP53 deletion was found in these gastric lesions, but p53-positive immunoreactivity was detected in 45% （5/11） and 12% （2/17） of CG and GU cases, respectively. However, there was no significant association between p53 expression and H pylori infection. CONCLUSION： The occurrence of aneuploidies in benign lesions evidences chromosomal instability in early stages of gastric carcinogenesis associated with Hpylori infection, which may confer proliferative advantage. The increase of p53 protein expression in CG and GU may be due to overproduction of the wild-type protein related to an inflammatory response in mucosa.展开更多
AIM： To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.METHODS： Seventy two patients were enrolled; 35 with duodenal, 22 with gastric ulcer and 26 with chronic gastritis. Patients...AIM： To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.METHODS： Seventy two patients were enrolled; 35 with duodenal, 22 with gastric ulcer and 26 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-2 and TNF~ were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score.RESULTS： Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis, sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median （± SE） sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment （203.21 ± 88.91 pg/1000 cells） compared to supernatants either from the same patients post-treatment （8.23 ± 5.79 pg/1000 cells） or from patients with chronic gastritis （6.21 ± 0.71 pg/1000 cells） （P 〈 0.001 and 〈 0.001, respectively）. Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients （P = 0.001）. Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes.CONCLUSION： sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer, sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.展开更多
基金Supported by the Brazilian Agency FAPESP,No.00/09413-6
文摘AIM： To investigate the occurrence of chromosome 3, 7, 8, 9, and 17 aneuploidies, TPS3 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H pylori infection. METHODS： Gastric biopsies from normal mucosa （NM, n = 10）, chronic gastritis （CG, n = 38）, atrophic gastritis （CAG, n=13） and gastric ulcer （GU, n=21） were studied using fluorescence in situ hybridization （FISH） and immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect Hpylori. An association of the gastric pathologies and aneuploidies with Hpylori infection was assessed. RESULTS： Aneuploidies were increasingly found from CG （21%） to CAG （31%） and to GU （62%）, involving mainly monosomy and trisomy 7, trisomies 7 and 8, and trisomies 7, 8 and 17, respectively. A significant association was found between H pylori infection and aneuploidies in CAG （P=0.0143） and GU （P=0.0498）. No TP53 deletion was found in these gastric lesions, but p53-positive immunoreactivity was detected in 45% （5/11） and 12% （2/17） of CG and GU cases, respectively. However, there was no significant association between p53 expression and H pylori infection. CONCLUSION： The occurrence of aneuploidies in benign lesions evidences chromosomal instability in early stages of gastric carcinogenesis associated with Hpylori infection, which may confer proliferative advantage. The increase of p53 protein expression in CG and GU may be due to overproduction of the wild-type protein related to an inflammatory response in mucosa.
文摘AIM： To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.METHODS： Seventy two patients were enrolled; 35 with duodenal, 22 with gastric ulcer and 26 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-2 and TNF~ were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score.RESULTS： Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis, sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median （± SE） sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment （203.21 ± 88.91 pg/1000 cells） compared to supernatants either from the same patients post-treatment （8.23 ± 5.79 pg/1000 cells） or from patients with chronic gastritis （6.21 ± 0.71 pg/1000 cells） （P 〈 0.001 and 〈 0.001, respectively）. Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients （P = 0.001）. Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes.CONCLUSION： sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer, sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.
