This study examined the effects of eradication of Helicobacter pylori (H pylon) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n= 8) and (b) patients with severe enlargement (>10 mm, n=8). After successful treatment, gastric body fold width was reduced in both groups (p<001) with an associated decrease in inflammatory infiltrates in the body mucosa (p<0.01 and p<0 05).Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1*1 (0.5) to 2*9 (0.9) mmol/h (p<005) and from 5-4 (1.3) to 18-7 (2.3) mmol/h (p<0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127-1 (16.1) to 59-6 (3.8) pg/ml (p<0.01). The increase in acid secretion after eradication of Hpylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p<0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0-91 (0.17) to 0 37 (0.08) mmol/h, p<005) and stimulated gastric secretions (from 1-57 (0.19) to 0 37 (0.13) mmol/h, p<001), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

A significant association is suggested between enlarged-fold gastritis and gastric carcinoma.

Background and Aims-It has been reported that eradication of Helicobacter pylon improves fold width in H pylon associated enlarged fold gastritis. The aim of this study was to clarify the mechanism of fold thickening in this condition. Patients and Methods-In eight patients with enlarged fold gastritis and 13 patients without enlarged folds, the presence of H pylori infection, inflammatory infiltrates, mucosal plasia, and epithelial cell proliferation in the body mucosa were investigated, and production of transforming growth factor a (TGFa), hepatocyte growth factor (HGF), and interleukin 1p (IL 1,) was determined by a competitive reverse transcription/polymerase chain reaction method and in vitro short-term culture ofbiopsy specimens. Results

Background/Aim-Helicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H pylori associated enlarged fold gastritis, suggesting that H pylori infection aVects parietal cell function in the gastric body. The aim of this study was to evaluate the eVects of H pylori infection on parietal cell morphology and function in hypochlorhydric patients. Patients/Methods-The presence of H pylori infection, mucosal length, and inflammatory infiltration were investigated in six patients with enlarged fold gastritis and 12 patients without enlarged folds. Parietal cell morphology was examined by immunohistochemistry using an antibody against the subunit of H + ,K + -ATPase and electron microscopy. In addition, gastric acid secretion and fasting serum gastrin concentration were determined before and after the eradication of H pylori. Results-In the H pylori positive patients with enlarged fold gastritis, fold width, foveolar length, and inflammatory infiltration were increased. In addition, the immunostaining pattern of H + , K + -ATPase was less uniform, and the percentage of altered parietal cells showing dilated canaliculi with vacuole-like structures and few short microvilli was greatly increased compared with that in H pylori positive patients without enlarged folds. After eradication, fold width, foveolar length, and inflammatory infiltrates decreased and nearly all parietal cells were restored to normal morphology. On the other hand, altered parietal cells were negligible in H pylori negative patients. In addition, the basal acid output and tetragastrin stimulated maximal acid output increased significantly from 0.5 (0.5) to 4.1 (1.5) mmol/h and from 2.5 (1.2) to 13.8 (0.7) mmol/h (p<0.01), and fasting serum gastrin concentrations decreased significantly from 213.5 (31.6) to 70.2 (7.5) pg/ml (p<0.01) after eradication in patients with enlarged fold gastritis. Conclusion-The morphological changes in parietal cells associated with H pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis. (Gut 1999;45:653-661)

Study design: An in vivo study in mouse models of spinal cord contusion. Objectives: To develop a novel indicator to anticipate the severity of spinal cord injury (SCI) during the acute phase and for the assessment of the efficacy of novel therapies. MicroRNAs (miRNAs) circulating in the peripheral blood are reported to modulate signaling between cells, and to be diagnostic markers for cancers. The purpose of this study was to identify circulating miRNAs for predicting the severity of SCI in the acute phase. Setting: Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Methods: Mouse SCI models were made using Infinite Horizon impactor with 50 or 70 kdyn compressing power following thoracic laminectomy. The mice were then divided into four groups: normal (without surgery), sham (laminectomy only), mild (50 kdyn), and severe (70 kdyn). TaqMan low-density array analysis and real-time PCR were performed to identify candidate miRNAs that were increased in the serum relative to the severity of SCI. Results: The expression levels of miR-9*, miR-219 and miR-384-5p in the serum were significantly increased relative to the severity of SCI 12 h after injury. The expression of miR-9* was also significantly increased relative to injury severity at 3 and 24 h after injury. Conclusion: Serum miR-9*, miR-219 and miR-384-5p might be promising biomarkers for predicting the severity of SCI.