Changing systems to address elder abuse: examples from aging services, the courts, the long-term care ombudsman, and the faith community.

The authors describe their use of systems change as a means of ameliorating elder abuse. After assessing the needs of their target audiences, projects developed a variety of strategies. These include disseminating promising practices in courts, creating Elder Law Clinics to assist with conservatorships, educating older adults about predatory mortgage lending, building a new response system for complaints of abuse and neglect in unlicensed care facilities, and convening clergy and lay leader groups to learn how faith communities can make a difference in elder abuse and neglect. The authors share tips on replicating their work, describing barriers to implementation and possible solutions.

Gastric mucosal cytokine and epithelial cell responses to Helicobacter pylori infection in Mongolian gerbils.

Experimental infection with Helicobacter pylori in Mongolian gerbils results in chronic gastritis and gastric cancer. To investigate epithelial cell proliferation, apoptosis, and mucosal cytokine responses in gastritis, Mongolian gerbils were infected with the H pylori SS1 strain. At 4 weeks post-infection, gastritis was predominantly within the antrum, but extended to the corpus in approximately 50% of gerbils by 36 weeks. Epithelial cell proliferation and apoptosis in glandular epithelial cells were increased with infection. Antral cell proliferation, but not apoptosis, correlated significantly with gastric inflammation. In female gerbils, H pylori significantly increased expression of transcripts for IFN-gamma and IL-12p40, but not TGF-beta or IL-10, in the gastric mucosa. Significantly reduced IFN-gamma and IL-12p40 responses were observed in male gerbils infected with H pylori, but epithelial proliferative and apoptotic responses were comparable to those of females. These studies demonstrate that the female gerbil cytokine response to H pylori has a Th1 profile and that there are gender differences in the magnitude of the gastric cytokine responses to H pylori. The absence of a down-regulatory cytokine response may account for the more severe gastritis observed with H pylori infection in gerbils than in mice.

Infection of Mongolian gerbils with Chinese Helicobacter pylori strains.

To date only a few Helicobacter pylori strains have been demonstrated to colonise Mongolian gerbils successfully. The aim of this study was to establish stable colonisation of Chinese strains of H. pylori in gerbils. Fresh clinical isolates from Chinese patients were inoculated into gerbils. At 4-6 weeks post inoculation, infection status was evaluated by culture, biopsy urease test and pathology. Sequencing of glmM and random amplified polymorphic DNA (RAPD) fingerprinting of DNA from cultured H. pylori were used to evaluate the genetic identity of pre-inoculated and post-inoculated strains. The ability of pre- and post-inoculated strains to stimulate interleukin-8 transcription in L5F11 gastric epithelial cells was analysed. Three of five clinical isolates colonised gerbils. The three pre- and post-inoculation strains had identical glmM sequences and RAPD profiles, and stimulated luciferase secretion from L5F11 epithelial cells. The strain that caused severe pathological changes was selected for repeat infection to prove reproducible and stable colonisation. The cagA+ strain 42GX gave stable colonisation in the gerbil and induced severe gastritis.

Gastric Helicobacter species infection in murine and gerbil models: comparative analysis of effects of H. pylori and H. felis on gastric epithelial cell proliferation.

C57BL/6 mice and Mongolian gerbils were infected with Helicobacter felis and Helicobacter pylori SS1 strain to investigate the effects of different Helicobacter species on gastric inflammation and epithelial cell proliferation in different animal models. At 4 weeks, gerbils infected with H. pylori or H. felis developed antral gastritis. Onset of gastritis varied between the models, with mice infected with H. pylori having minimal inflammation at 8 weeks. In mice, H. felis, but not H. pylori, induced significantly increased epithelial cell proliferation in the cardia and corpus at 8 weeks, but no changes were observed at 4 weeks. In gerbils, both H. pylori and H. felis significantly increased antral epithelial cell proliferation at 4 weeks. Epithelial cell proliferation induced by H. felis in gerbils was twice that stimulated by H. pylori. These studies demonstrate host differences in the development of Helicobacter species-induced gastric inflammation and a marked difference in epithelial cell proliferation induced by H. pylori and H. felis in 2 animal models.