Kazuhide Higuchi

Mechanisms and Roles of Neutrophil Infiltration in Stress-Induced Gastric Injury in Rats

Water-immersion and restraint stress is associated with an increase in neutrophil infiltration into the gastric mucosa, but the mechanism responsible for this infiltration is unclear. We investigated the involvement of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α) in neutrophil infiltration in stress-induced gastric injury in rats. Rats were administered neutralizing antibody against ICAM-1 or TNF-α and were subjected to induction of gastric injury by 6-hr water-immersion and restraint stress. To evaluate the relationship between gastric acid and neutrophil infiltration, some rats were given cimetidine before administration of stress. Neutralizing antibodies inhibited both the lesion formation and the increase in myeloperoxidase activity induced by stress. Expression of ICAM-1 on endothelial cells was increased by stress, accompanied by an increase of TNF-α-positive cells. Antibody against TNF-α inhibited this increase in ICAM-1 expression. Cimetidine almost completely inhibited gastric lesions, but did not affect myeloperoxidase activity. In conclusion, neutrophil infiltration in stress-induced gastric injury may be mediated by ICAM-1 and TNF-α, but not gastric acid, and may play crucial roles in the progression of gastric injury.

Is eradication sufficient to heal gastric ulcers in patients infected with Helicobacter pylori? A randomized, controlled, prospective study

Background : In Helicobacter pylori infection, the effect of short‐term triple therapy with proton pump inhibitor plus two antibiotics on gastric ulcer healing is not well known.

Efficacy and safety of balloon-occluded endoscopic injection sclerotherapy as a prophylactic treatment for high-risk gastric fundal varices: A prospective, randomized, comparative clinical trial ☆

BACKGROUND No single effective method has yet been established for the prophylactic treatment of gastric fundal varices at high risk for bleeding. A prospective, randomized trial was conducted to compare the efficacy and safety of a new technique, balloon-occluded endoscopic injection sclerotherapy (BO-EIS), to balloon-occluded retrograde transvenous obliteration (B-RTO) for treatment of high-risk gastric fundal varices. METHODS Twenty consecutive patients with gastric variceal diameters of over 5 mm by color Doppler EUS were randomized to undergo either BO-EIS or B-RTO. All patients underwent color Doppler EUS 2 weeks after treatment and EGD every 3 months for assessment of sclerosing effect. RESULTS The gastric varices in all patients except one in the B-RTO group were eradicated with either treatment. The volume of sclerosant used was significantly smaller in patients who underwent BO-EIS (p < 0.05). The endoscopic grade of esophageal varices in 4 of 9 patients worsened after treatment with B-RTO (p < 0.05). The method of randomization used resulted in an uneven distribution of women, although the difference between the groups was not statistically significant. When only men were compared, the results of the study were unchanged. CONCLUSIONS BO-EIS is a safe and effective for treatment of high-risk gastric fundal varices. In contrast to B-RTO, it can be used even in patients without a gastrorenal shunt.

ERADICATION OF HELICOBACTER PYLORI WITH A CHINESE HERBAL MEDICINE WITHOUT EMERGENCE OF RESISTANT COLONIES

Eradication of Helicobacter pylori With a Chinese Herbal Medicine Without Emergence of Resistant Colonies

Is Helicobacter pylori-negative duodenal ulcer masked by the high prevalence of H. pylori infection in the general population?

Is Helicobacter pylori -Negative Duodenal Ulcer Masked by the High Prevalence of H. pylori Infection in the General Population?

Induction of signal transduction pathways in rat gastric epithelial cells stimulated with interleukin‐1β

Background: Interleukin‐1β (IL‐1β) participates in cell growth, differentiation and apoptosis via activation of several kinases in a variety of cells. Mitogen‐activated protein (MAP) kinases are important intermediates of the signal transduction pathway from the cell surface to the nucleus, leading to activation of transcription factors. There are no reports on the effect of IL‐1β on these pathways in gastric epithelial cells.

Overexpression of co-stimulatory molecules in peripheral mononuclear cells of Helicobacter pylori-positive peptic ulcer patients: possible difference in host responsiveness compared with non-ulcer patients.

Background/Aim Helicobacter pylori is the principal cause of gastritis and peptic ulcer disease. However, H. pylori-positive patients do not always have peptic ulcer. This study was carried out in order to determine the difference in host immune reaction to H. pylori between patients with peptic ulcer and those without. Methods Ten H. pylori-positive patients with peptic ulcer, 10 H. pylori-positive non-ulcer patients, and 10 healthy volunteers were examined for expression of surface molecules in peripheral blood mononuclear cells. The surface molecules were stained with immunofluorescence-labelled specific antibodies and analysed by flow cytometry. Results More mononuclear cells expressed molecules ICAM-1, VLA-4, Leu-M3 in H. pylori-positive ulcer patients than in non-ulcer patients and healthy volunteers. There were also more cells expressing CD28, SLex, CD4, HLA-DR, and NU-B2 in H. pylori-positive ulcer patients than in non-ulcer patients and healthy volunteers. There were fewer cells expressing CD8 in H. pylori-positive ulcer patients than in non-ulcer patients and healthy volunteers. Conclusion H. pylori infection may cause immunological reactions which are reflected in peripheral mononuclear cells. However, the activity and characteristics of peripheral mononuclear cells, in terms of expression of adhesion molecules, may differ between ulcer and non-ulcer patients who are infected with H. pylori.

Marked Enhancement by Fish Meal of Helicobacter pylori‐induced Gastritis in Mongolian Gerbils

In a search for dietary factors influencing Helicobacter pylori‐induced gastritis, the effects of fish meal in the diet were examined in Mongolian gerbils. When a conventional diet containing 10% fish meal was given to Mongolian gerbils for 4 weeks after inoculation of H. pylori, edematous thickening with severe neutrophil and mononuclear cell infiltration in both the mucosa and submucosa was observed in the glandular stomach of 19 out of the 20 animals, and hemorrhagic spots were evident in 11 cases. These gastric lesions were enhanced by a 20% fish meal supplement, and edema and hemorrhage in the gastric mucosa were observed in 19 and 17 out of 20 animals, respectively. Although almost the same levels of viable bacteria were detected independent of the diet, edema and hemorrhage were seen in only 2 and 1 of 20 gerbils fed a diet containing 10% casein, instead of 10% fish meal, respectively. Neither edema nor hemorrhage was observed in 10% beef diet animals. These results suggest that fish meal contains factors which greatly enhance H. pylori‐induced gastritis in Mongolian gerbils. Since the incidences of gastritis and gastric cancer are very high throughout the world, it is very important to identify these gastritis‐enhancing factors.

High molecular protein of Helicobacter pylori responsible for inhibition of ornithine decarboxylase activity of human gastric cultured cells

Ornithine decarboxylase (ODC), a rate‐limiting enzyme of polyamine biosynthesis, mediates epithelial cell proliferation and plays a critical role in the optimal repair of gastric mucosal damage. Several studies have shown that Helicobacter pylori inhibits the growth and proliferation of gastric cells in vitro.

Risk associated with reprocessed reusable endoscopic instruments

derwent laparotomy, loop ileostomy, and proctocolectomy after 4 days of intractable rectal bleeding. Histological examination of the surgical specimen identified high-grade non-Hodgkin’s B-cell lymphoma of the mucosa-associated lymphoid tissue type. A staging investigation including chest x-ray, thoracic and abdominal CT scan, schintigraphy of the skeleton, and examination of the bone marrow did not reveal further involvement; a diagnosis of primary colorectal lymphoma was made. The patient has been observed to the present time, with no evidence of recurrent lymphoma. Cytomegalovirus is a herpesvirus that can induce several hematological and immunological disorders that may culminate in increased susceptibility of the involved tissue to malignant degeneration. It has an array of immune escape strategies like inhibiting major histocompatibility complex class I expression and blockage of the interferon –induced major histocompatibility complex class II–dependent antigen presentation; these in turn may enhance its ability to establish long-lasting latent state and host DNA alterations. Moreover, it may induce proinflammatory changes by expansion of CD8 T cells and natural killer cells (2). Additionally, it has been reported that cytomegalovirus can exacerbate inflammatory bowel disease, causing destruction and ulceration of epithelial and endothelial cells, myocytes, and fibroblasts (3). Interestingly, it has been implicated in cases of resistance to medical therapy, which is not dependent on reduction in either glucocorticoid receptor avidity or DNA affinity. The various mechanisms of pathogenesis of GI lymphoma include lymphoid hyperplasia, prolonged stimuli to mucosa-associated lymphoid tissue, prolonged use of corticosteroids and azathioprine, severe (38% vs 10%) and longstanding (80% vs 35%) UC (4). All of which may apply to cytomegalovirus infection. We would like to know how many patients developed lymphoma in this series and whether the authors have data comparing the incidence of lymphoma in this series to a comparable group of patients with non–cytomegalovirus infected UC.