T. Masaoka

Helicobacter pylori infection modifies gastric and plasma ghrelin dynamics in Mongolian gerbils

Background and aim: Although ghrelin, a novel growth hormone releasing peptide localised mainly in the gastric fundus, is reported not only to accelerate food passage and gastrointestinal motility but also to affect appetite and weight control, regulation of gastric ghrelin secretion under the conditions of gastric Helicobacter pylori infection is unknown. The present study was designed to investigate plasma and gastric ghrelin levels in Mongolian gerbils with H pylori colonisation of the gastric mucosa. Methods: Gerbils orally inoculated with H pylori were examined after inoculation. To examine preproghrelin mRNA expression in the gastric mucosa, cDNA encoding the gerbil preproghrelin and glyceraldehyde-3-phosphate dehydrogenase homologue was isolated and a quantitative reverse transcription-polymerase chain reaction system was established. Results: In gerbils showing H pylori colonisation (H pylori group), expression of preproghrelin mRNA and total ghrelin levels were significantly decreased 17 and 23 weeks later (p<0.01). Although the number of ghrelin immunoreactive cells decreased as the stomach weight increased, the gastric contents of total and active ghrelin in this group were the same as those in controls. Gastric myeloperoxidase activity showed a positive correlation with plasma ghrelin levels. On the other hand, at 17 weeks, plasma ghrelin levels were significantly increased in the H pylori group (p<0.05), suggesting a compensatory increase in secretion of the peptide at this time point. Conclusion: The present experimental study demonstrated that gastric and plasma ghrelin dynamics are altered in response to H pylori infection.

Second-line treatment of Helicobacter pylori infection after dilution agar methods and PCR-RFLP analysis

Background :u2002After unsuccessful first‐line treatment of Helicobacter pylori infection, the percentage of clarithromycin‐resistant strains has been reported as between 30% and 70% in Japan and other countries. A high prevalence of clarithromycin‐resistant strains is reported to be associated with eradication failure.

Enhanced plasma ghrelin levels in patients with functional dyspepsia: ENHANCED PLASMA GHRELIN LEVELS IN FUNCTIONAL DYSPEPSIA

Ghrelin, growth‐hormone‐releasing peptide, has been reported to accelerate food intake and gastrointestinal motility.

Intravenous ghrelin administration enhances gastric acid secretion - evaluation using wireless pH capsule: ROLE OF GHRELIN IN GASTRIC ACID SECRETION

Ghrelin, a recently discovered peptide hormone, has been shown to be produced mainly by the A‐like cells of the gastric mucosa. Ghrelin not only stimulates growth hormone (GH) release but also promotes gastric motility. While the effect of ghrelin on the gastric acid secretion in rats has been reported, no such reports appeared to date from studies in humans.

Could frameshift mutations in the frxA and rdxA genes of Helicobacter pylori be a marker for metronidazole resistance?: FRXA AND RDXA GENES TO METRONIDAZOLE RESISTANCE IN H. PYLORI

Although resistance of Helicobacter pylori to metronidazole had been reported to be associated with mutations in the rdxA or the frxA gene, recent studies have indicated that they may contribute little to metronidazole resistance.

Increased levels of plasma ghrelin in peptic ulcer disease: GHRELIN AND PEPTIC ULCER

Ghrelin is a novel appetite‐promoting peptide secreted primarily from the A‐like cells in the gastric fundic mucosa. As gastric inflammation caused by Helicobacter pylori infection extends, the number of ghrelin‐producing A‐like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non‐ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine‐induced duodenal ulcer.

Evaluation of the role of Helicobacter pylori as a promoter of gastric cancer from the viewpoint of structural chromosomal aberration: H. PYLORI INFECTION AND STRUCTURAL CHROMOSOMAL ABERRATION

To examine whether Helicobacter pylori induces structural chromosomal aberrations, such as loss of heterozygosity (LOH) and microsatellite instability (MSI) in the infected gastric mucosa.

Role of perforin and granzyme B of cytotoxic T lymphocyte in the onset of peptic ulcer formation

Attention has been focused on apoptosis in terms of its involvement in the pathogenesis of various diseases including hepatitis, graft-versus-host disease (GVHD), and multiple sclerosis [1–3]. Some pathways are known to be implicated in cytotoxic T lymphocyte (CTL)-mediated apoptotic induction: perforin/granzyme pathway (based on granules stored in cytoplasmic azurophile granules of CTLs), Fas/Fas ligand (FasL), tumor necrosis factor (TNF)/TNF receptor (TNFR), or TNF-related apoptosis-inducing ligand (TRAIL) pathways based on type II transmembrane proteins belonging to the TNF family expressed on the cell surface. Among them, the perforin/granzyme and Fas/FasL pathways are considered the two major routes of apoptosis. The aim of this study is to investigate whether apoptosis associated with peptic ulcer formation may occur via either or both of these two pathways.