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  • 1
    Electronic Resource
    Electronic Resource
    Synthesis and characterization of a branched-chain hexacarbene in a tridecet ground state. An approach to superparamagnetic polycarbenes (1992)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 114 (1992), S. 1484-1485 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00030a055
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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
    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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  • 4
    Electronic Resource
    Electronic Resource
    Enterocromaffin-Like Cell Tumor Induced by Helicobacter pylori Infection in Mongolian Gerbils (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. Gastric carcinoids are strongly associated with chronic atrophic gastritis A, and it is suggested that hypergastrinemia plays a critical role in development of gastric carcinoids. Since Helicobacter pylori infection causes hypergastrinemia, it is held that H. pylori infection produces gastric carcinoids. We followed the histological changes of H. pylori-infected stomachs of Mongolian gerbils for a long time.Materials and Methods. Five-week-old-male Mongolian gerbils were infected with H. pylori ATCC 43504 with cagA gene, expressing vacuolating cytotoxin. Determination of the serum gastrin and histopathological examination of the stomach at 6, 12, 18, and 24 months after H. pylori inoculation was studied and compared with uninfected animals.Results In infected animals, the gastric carcinomas appeared 18 and 24 months after infection. Endocrine cell dysplasias and carcinoids with marked atrophic gastritis of the oxyntic mucosa were observed in the infected animals 24 months after H. pylori inoculation. The serum gastrin level in the infected group increased from an average of 86.2 pg/ml at the beginning of the study to an average of 498 pg/ml and 989 pg/ml at 18 and 24 months after infection, respectively. These changes in the serum gastrin levels were significant compared with uninfected controls that showed no changes.Conclusions. H. pylori infection caused not only gastric carcinomas but also enterochromaffin-like cell tumors in Mongolian gerbils, due to hypergastrinemia. This model is thought to be useful to study the relationship between hypergastrinemia and gastric carcinoids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2002.00115.x
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  • 5
    Electronic Resource
    Electronic Resource
    A Multicenter, Double-Blind Study on Triple Therapy with Lansoprazole, Amoxicillin and Clarithromycin for Eradication of Helicobacter pylori in Japanese Peptic Ulcer Patients (2001)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 6 (2001), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Two triple therapies with lansoprazole (LPZ)/amoxicillin (AMPC)/clarithromycin (CAM) for eradication of Helicobacter pylori were studied in multicenter, double-blind fashion to evaluate the eradication rate of H. pylori and safety of eradiation treatment in Japanese patients with H. pylori-positive active gastric ulcers or duodenal ulcers.〈section xml:id="abs1-3"〉〈title type="main"〉Methods.Patients were randomly chosen for the control treatment of LPZ 30 mg twice a day (b.i.d.; Group A-LPZ-only) or the test treatments of LPZ 30 mg plus AMPC 750 mg and CAM 200 mg b.i.d. (Group B-LAC200) and LPZ 30 mg, AMPC 750 mg and CAM 400 mg b.i.d. (Group C-LAC400). All eradication treatments lasted for a period of 7 days. Successful eradication was assessed by culture and gastric histology 1 month after completion of the ulcer treatment.〈section xml:id="abs1-4"〉〈title type="main"〉Results.The eradication rates of H. pylori in the full analysis set were 0% in Group A-LPZ-only, 87.5% in Group B-LAC200 and 89.2% in Group C-LAC400 for gastric ulcer and, 4.4% in Group A-LPZ-only, 91.1% in Group B-LAC200 and 83.7% in Group C-LAC400 for duodenal ulcer. The eradication rates of Group B-LAC200 and Group C-LAC400 were 89.2% (95% CI: 84.8–93.7%) and 86.4% (95%CI: 81.5–91.3%) in total in the full analysis set, 89% (95% CI: 84.3–93.7%) and 85.3% (95%CI: 80.1–90.5%) in the per protocol set. The eradication rates in Groups B-LAC200 and group C-LAC400 were statistically significantly higher than the rate in Group A-LPZ-only for both gastric ulcer and duodenal ulcer patients (p 〈 .0001 for both).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion.A satisfactorily high H. pylori eradication rate was obtained in Japanese ulcer patients with the triple therapy regimen consisting of LPZ 30 mg, AMPC 750 mg, and CAM 200 mg b.i.d.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2001.00037.x
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  • 6
    Electronic Resource
    Electronic Resource
    Highly Sensitive Urine-Based Enzyme-Linked Immunosorbent Assay for Detection of Antibody to Helicobacter pylori (1998)
    Cambridge, MA, USA : Blackwell Publishing Ltd
    Helicobacter 3 (1998), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Enzyme-linked immunosorbent assay (ELISA) has been widely used for detection of Helicobacter pylori (H. pylori), but sample collection is often invasive, complicated, and expensive. Urine samples can be obtained noninvasively and are easier and safer to handle than serum samples. A urine-based ELISA, if found to be accurate, would therefore be a useful alternative to serum-based tests for H. pylori.〈section xml:id="abs1-2"〉〈title type="main"〉Methods.An ELISA method was developed for detection of antibodies to H. pylori in urine. Its sensitivity and specificity were compared with those of three commercially available serum-based ELISA kits and the 13C urea breath test (13C-UBT) using samples from 99 healthy volunteers and 20 patients with gastric disorders.〈section xml:id="abs1-3"〉〈title type="main"〉Results.With the assumption that 13C-UBT results are 100% accurate, the sensitivity and specificity of the urinary ELISA were 99% and 100%, respectively, and the accuracy (99%) was superior to those of the three serum ELISAs tested. Immunostaining profiles on Western blot analysis using serum samples were almost identical to those obtained using paired urine samples.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.These findings suggest that the differences observed among ELISA test results may be due principally to differences between the profiles of antigen coated on plates for the assays, rather than to differences between antibodies in serum and urine. The urine-based ELISA (URINELISA H. pylori) developed in this study is very accurate and would be useful for screening H. pylori infection as an alternative to serum ELISAs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.1998.08045.x
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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Effects ofHelicobacter pylori infection on gastric mucosal defense factors in Japanese monkeys (1995)
    Springer
    Journal of gastroenterology 30 (1995), S. 441-446 
    Details
    ISSN: 1435-5922
    Keywords: H. pylori ; gastric mucosal defense factor ; cell kinetics ; animal model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenic role played byHelicobacter pylori in gastric mucosal defense was investigated in Japanese monkeys infected withH. pylori. Serum gastrin levels and ammonia concentrations in gastric juice were compared inH. pylori-infected (n=6) and control (n=7) groups. The gastritis score, the intracellular content of periodic acid-Schiff (PAS)-positive substance and hexosamine, and the bromodeoxyuridine (BrdU) labeling index in the gastric mucosa were compared in the two groups in the antrum and the corpus. The ammonia concentration in the gastric juice was significantly higher in the infected group (P〈0.01). The gastritis scores were significantly higher in the antrum and corpus in the infected group (P〈0.01, andP〈0.05, respectively). The content of PAS-positive substance and hexosamine was significantly decreased in the antrum of the infected group compared with that in the controls (P〈0.01, andP〈0.05, respectively), but there was no significant difference between the two groups in the corpus. The BrdU labeling indices were significantly higher in the antrum and corpus of the infected group (P〈0.01, andP〈0.01, respectively). Colonization byH. pylori injures the gastric mucosa by depressing the gastric mucosal defense factors, and, consequently, the cell kinetics are accelerated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02347558
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  • 9
    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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  • 10
    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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