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  • 1
    Electronic Resource
    Electronic Resource
    Long-Term Helicobacter pylori Infection in Japanese Monkeys Induces Atrophic Gastritis and Accumulation of Mutations in the p53 Tumor Suppressor Gene (2002)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 7 (2002), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Helicobacter pylori is accepted as a definite human gastric carcinogen from an epidemiological point of view despite insufficient experimental data. Although we previously showed that the number of p53 immunopositive cells in the atrophic gastric mucosa of H. pylori-infected Japanese monkeys gradually increased over time, data on p53 gene mutations were not obtained in that study. To obtain direct evidence of carcinogenesis associated with H. pylori infection, we investigated whether p53 gene mutations are present in the gastric mucosa of a nonhuman primate model susceptible to H. pylori.Materials and Methods. Using the DNA from gastric tissues obtained from six H. pylori-uninfected monkeys of different ages, nucleotide sequence of the wild-type p53 gene was determined by amplification of exons (Ex) 5, 6, 7 and 8 and sequencing. Gastric specimens obtained from eight Japanese monkeys that had been infected with H. pylori for different lengths of time (1.5–7.5 years), were analyzed for mutations in exons 5–8 of p53.Results. In the six H. pylori-uninfected monkeys, nucleotide sequences of p53 Ex 5–8 were completely common and no mutations were noted. However, among the monkeys that were infected with H. pylori over various periods of time, there was an accumulation of p53 nucleotide (amino acid) substitutions as the gastric atrophy score increased.Conclusions. We conclude that the appearance of p53 gene mutation may be closely associated with the degree of gastric mucosal atrophy, which depends on the duration of H. pylori infection. Searching for p53 gene mutations may be useful for studying the progression of gastric carcinogenesis associated with H. pylori.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2002.00074.x
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  • 2
    Electronic Resource
    Electronic Resource
    Is the Recurrence of Helicobacter pylori Infection After Eradication Therapy Resultant from Recrudescence or Reinfection, in Japan (2003)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 8 (2003), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Reinfection of Helicobacter pylori after eradication is rare in developed countries but most often occurs within 1 year. In the present study, we attempted to differentiate between reinfection and recrudescence of H. pylori strains between 6 months and 6 years after successful eradication in Japan, a country with a high prevalence of H. pylori infection.Materials and Methods. After successful eradication of H. pylori, 274 patients were followed up by endoscopy and urea breath test. In recurrent patients, H. pylori strains isolated initially and after recurrence were compared using PCR-based restriction fragment length polymorphism (RFLP) analysis.Results. Recurrence of H. pylori occurred in 15 of 274 patients (5.5%) at 6 months after eradication and the annual recurrence rate was 2.0% per patient year (between 1 and 6 years). PCR-based RFLP analysis of H. pylori strains isolated initially and after recurrence showed that 62.5% (at 6 months) and 100% (after 1 years) of bacteria were of different strains.Conclusion. Reinfection of H. pylori was not as rare at 6 months after eradication as reported previously, and up to 6 years after eradication, the annual reinfection rate is 2.0% per patient year in Japan.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2003.00143.x
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of Osteopontin in a Macrophage Cell Line and in Transgenic Mice with Pulmonary Fibrosis Resulting from the Lung Expression of a Tumor Necrosis Factor-α Transgene (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 760 (1995), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1995.tb44651.x
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  • 4
    Electronic Resource
    Electronic Resource
    Efficacy of recombinant human granulocyte-colony stimulating factor alone and in combination with antifungal agents against disseminated trichosporonosis in neutropenic mice (1996)
    Springer
    Journal of infection and chemotherapy 2 (1996), S. 232-239 
    Details
    ISSN: 1437-7780
    Keywords: trichosporonosis ; neutropenic mice ; rhG-CSF ; antifungal agents
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of recombinant human granulocyte colony-stimulating factor (rhG-CSF) to protect and potentiate the activity of antifungal agents against a lethalTrichosporon beigelii infection in myelosuppressed mice was evaluated in this study. Mice were rendered neutropenic by 2 consecutive-day intraperitoneal injections of cyclophosphamide (200 mg/kg). Recombinant hG-CSF, given subcutaneously at daily doses of 15, 60, and 120 μg/kg for 6 days, shortened the period of neutropenia and increased the number of circulating neutrophils in a dose-dependent manner. When rhG-CSF was administered to neutropenic mice before challenge withT. beigelii (5×106 CFU), it protected against the lethal infection, resulting in improved survival and decreased numbers of fungal cells in the lung, liver, spleen and kidney. However, when the inoculum size increased to 7×106 CFU, a poorer result was obtained using a dose of 60 μg/kg of rhG-CSF, suggesting that the activity of rhG-CSF is dependent on the severity of theT. beigelii infection. Combined with fluconazole (10 mg/kg) or amphotericin B (1 mg/kg), rhG-CSF improved the median survival time from 16 days with fluconazole (59%) and 12 days with amphotericin B (41%) alone to 20 days (93%) and 16 days (55%) in neutropenic mice treated with rhG-CSF plus fluconazole or amphotericin B, respectively. However, the combination of rhG-CSF and itraconazole did not produce significant improvement in survival or clearance of fungal cells from the organs of neutropenic mice. These findings show that rhG-CSF may be a useful immunomodulator againstTrichosporon infections in neutropenic mice and the therapeutic outcome improves when used in combination with fluconazole or amphotericin B.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02355120
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  • 5
    Electronic Resource
    Electronic Resource
    Helicobacter pylori-infected Japanese monkeys (1995)
    Springer
    Journal of infection and chemotherapy 1 (1995), S. 90-97 
    Details
    ISSN: 1437-7780
    Keywords: Helicobacter pylori ; japanese monkey ; gastritis ; peptic ulcer ; gastric cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion It is possible to establish persistentH. pylori infection in the gastric mucosa of Japanese monkeys and create acute and chronic gastritis similar to that found in humans; persistent infection causes atrophic changes in the gastric mucosa. Japanese monkeys, which age approximately flve times faster than humans, provide a valuable model for investigating the long-term effects ofH. pylori infection on the gastric mucosa and for the study of stages in the development of gastric cancer. H. pylori produces gastritis resulting in both local inflammation and a systemic immune response. Genes have been isolated that code for cytotoxic proteins such as CagA, VacA, and for heat-shock protein. A number of points remain unresolved concerning the pathology ofH. pylori infection, known to be closely related to the recurrence of peptic ulcers. Routes of infection are fecaloral and oral-oral, and humans can be infected from pets.53 Gastroendoscopy can be a source of nosocomial infections. The natural habitat ofH. pylori in humans is limited almost exclusively to the surface layer of the gastric mucosa; it is rarely found in other locations. In the future, we should develop chemotherapeutic methods for curingH. pylori infections and a vaccine for their prevention. The present study was conducted in accordance with Oita Medical University guidelines for animal experimentation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02348751
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  • 6
    Electronic Resource
    Electronic Resource
    Molecular typing ofHelicobacter pylori: Differences in pathogenicity among diverse strains (1996)
    Springer
    Journal of gastroenterology 31 (1996), S. 1-5 
    Details
    ISSN: 1435-5922
    Keywords: Helicobacter pylori ; polymerase chain reaction-restriction fragment length polymorphism ; urease activity ; strain diversity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Helicobacter pylori appears to be a species with strain diversity, according to studies carried out using various molecular biological techniques. Differences in pathogenicity caused by the strain diversity ofH. pylori were therefore investigated. Two hundred and thirty strains were divided into four types by polymerase chain reaction-restriction fragment length polymorphism, and their relationship to endoscopic diagnosis, ammonia concentration of gastric juice, and urease activity were assessed. With regard to incidence by type, patients infected with type 1, type 2, and type 3 exhibited the highest incidences of gastric ulcer, duodenal ulcer, and gastritis, respectively. The urease activity of type 2 was significantly lower than that of types 1 and 3 (P〈0.05). These observations suggest differences in pathogenicity due to the strain diversity ofH. pylori. However, the diversity of diseases related toH. pylori is also presumed to be caused by both the diversity ofH. pylori strains and differences in the host immunological reaction. Future studies should be directed toward clarifying the entire pathogenic mechanism ofH. pylori infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01211179
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of ethanol on the pancreas of disulfiram-treated rats (1995)
    Springer
    Journal of gastroenterology 30 (1995), S. 231-236 
    Details
    ISSN: 1435-5922
    Keywords: disulfiram ; ethanol ; acetaldehyde ; lipid inclusions ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To study the effects of ethanol on disulfiram-treated rats, we administered ethanol orally at a does of 2000 mg/kg, twice daily for 5 days. The administration of ethanol or disulfiram alone produced no recognizable changes in pancreatic acinar cells. Ethanol administration. in disulfiram-treated rats resulted in a decrease in the content of zymogen granules in acinar cells, and the appearance of intraplasmic vacuolization. Electron microscopically, these vacuoles appeared on the basal side of nuclei. In addition, similar vacuoles appeared in liver cells, and these vacuolizations seemed to show lipid inclusions. However, ethanol administration to disulfiram-treated rats did not cause inflammatory changes or edema in the pancreas. A comparison of blood ethanol levels in rats receiving ethanol alone and disulfiram plus ethanol showed no significant difference, but acetaldehyde levels in rats receiving ethanol plus disulfiram rats were significantly higher than those in rats receiving ethanol alone. These findings suggested that acetaldehyde caused a decrease of zymogen granules and the presence of lipid inclusions in pancreatic acinar cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02348670
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