• Title/Summary/Keyword: Helicobacter

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Risk of the Gastric Cancer Associated with the Interleukin $1\beta$ Gene Polymorphism and Helicobacter pylori (Helicobacter pylori 감염과 Interleukin $1\beta$ 유전자의 다형성에 따른 위암 발생 위험도)

  • Park, Sang-Hyub;Song-Kyo-Young;Kim, Jin-Jo;Jin-Hyung-Min;Kim, Wook;Park, Cho-Hyun;Park, Seung-Man;Lim-Keun-Woo;Park, Woo-Bae;Kim, Seung-Nam;Jeon, Hae-Myung
    • Journal of Gastric Cancer
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    • v.4 no.3
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    • pp.149-155
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    • 2004
  • Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1\beta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1\beta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1\beta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1\beta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1\beta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26\∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81\~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1\beta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.

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Helicobacter Species are Possible Risk Factors of Cholangiocarcinoma

  • Kaewpitoon, Soraya J;Loyd, Ryan A;Rujirakul, Ratana;Panpimanmas, Sukij;Matrakool, Likit;Tongtawee, Taweesak;Kootanavanichpong, Nusorn;Pengsaa, Prasit;Kompor, Ponthip;Chavengkun, Wasugree;Kujapun, Jirawoot;Norkaew, Jun;Ponphimai, Sukanya;Padchasuwan, Natnapa;Polsripradist, Poowadol;Eksanti, Thawatchai;Phatisena, Tanida;Kaewpitoon, Natthawut
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.1
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    • pp.37-44
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    • 2016
  • Several infectious agents are considered to be causes of cancer in human, mainly hepatitis B and C viruses, high-risk human pailloma viruses, Helicobacter pylori, Clonorchis sinensis, and Opisthorchis viverrini. Here we described the evident research and the association between Helicobacter spp. and biliary tract cancer particularly cholangiocarcinoma (CCA). Global epidemiological studies have suggested that Helicobacter spp. are possible risk factors for biliary tract diseases. Molecular studies support a linkage of Helicobacter spp. with CCA development. H. pylori, H. bilis, and H. hepaticus, are found in CCA, but the most common species are H. pylori and H. bilis. The type of CCA are associated with Helicobacter spp. include extrahepatic CCA, and common bile duct cancer. Up to the present, however, the results from different regions, materials and methods, sub-sites of cancer, and controls have not been consistent, thus introducing heterogeneity. Therefore, a comparison between co-Helicobacter spp.-CCA in the countries with low and high incident of CCA is required to settle the question. Furthermore, clarifying variation in the role of Helicobacter species in this CCA, including pathogenesis of CCA through enhanced biliary cell inflammation and proliferation, is necessary.

The Prevalence of Atrophic Gastritis and Intestinal Metaplasia according to Gender, Age and Helicobacter Pylori Infection in a Rural Population (한 농촌지역 주민에서 성, 연령 및 Helicobacter pylori 감염 여부에 따른 위축성 위염과 장상피화생 유병률)

  • Kim, Hyun-Ja;Choi, Bo-Youl;Byun, Tae-Joon;Eun, Chang-Soo;Song, Kyu-Sang;Kim, Yong-Sung;Han, Dong-Soo
    • Journal of Preventive Medicine and Public Health
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    • v.41 no.6
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    • pp.373-379
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    • 2008
  • Objectives ; The objective of this study was to evaluate the prevalence of atrophic gastritis and intestinal metaplasia according to gender, age and Helicobacter pylori infection in a rural population in Korea. Methods: Between April 2003 and January 2007, 713 subjects (298 men and 415 women, age range: 18-85) among the 2,161 adults who participated in a population-based survey received gastrointestinal endoscopy. All the subjects provided informed consent. Multiple biopsy specimens were evaluated for the presence of atrophic gastritis and intestinal metaplasia. The presence of Helicobacter Pylori was determined using CLO and histology testing. Results ; The age-adjusted prevalence of atrophic gastritis was 42.7% for men and 38.1% for women and the prevalence of intestinal metaplasia was 42.5% for men and 32.7% for women. The prevalence of atrophic gastritis and intestinal metaplasia increased significantly with age for both men and women (p for trend<0.001). The age-adjusted prevalence of Helicobacter pylori was similar for men (59.0%) and women (56.7%). The subjects with Helicobacter pylori infection showed a significantly higher prevalence of intestinal metaplasia (44.3%) compared with that (26.8%) of the noninfected subjects (p<0.001). However, the prevalence of atrophic gastritis was not statistically different between the Helicobacter pylori-infected subjects and the noninfected individuals. Conclusions : Our findings suggest that the prevalence of atrophic gastritis and intestinal metaplasia is higher for a Korean rural population than that for a Western population; this may be related to the high incidence of gastric cancer in Koreans. Especially, the prevalence of intestinal metaplasia was high for the subjects with Helicobacter pylori infection. The multistep process of gastric carcinogenesis and the various factors contributing to each step of this process need to be determined by conducting future follow-up studies.

Production of Inhibitory Compounds against Helicobacter pylori by Culture Condition of Morus alba cv. Cheongmoknosang Callus (청목노상(Morus alba cv. Cheongmoknosang) callus의 배양조건에 따른 Helicobacter pylori 억제물질의 생산)

  • Cho, Young-Je;Cha, Won-Seup;Kang, Sun-Ae;An, Bong-Jeun;Ahn, Dong-Hyun;Kim, Myung-Uk;Chae, Jung-Woo
    • Journal of Life Science
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    • v.23 no.3
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    • pp.368-376
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    • 2013
  • The optimal condition for Morus alba cv was an MS culture medium at $27^{\circ}C$ for 20 days. Cheongmoknosang callus showed inhibitory activity against Helicobacter pylori at 1.05 g of wet weight of the cultured callus. The callus formation of Morus alba cv. Cheongmoknosang was influenced by naphthalene acetic acid (NAA), 2,4-dichlorophenoxy acetic acid (2,4-D), 6-benzylaminopurine (BA) and kinetin at concentrations of 2 mg/l. The growth rate of callus was higher than it was when these hormones were mixed with a single hormone. Thus, the optimal condition for direct callogenesis was to incubate with mixture (2,4-D/NAA) of 2 mg/l concentration at $27^{\circ}C$ for 20 days. Moreover, the optimal culture condition of the biomass in the mass production of inhibitory compounds against Helicobacter pylori from Morus alba cv. Cheongmoknosang callus was to incubate in an MS broth (each concentration 1 mg/l of 2,4-D and BA). When Morus alba cv. Cheongmoknosang callus were incubated for 20 days in a bioreactor, Helicobacter pylori inhibition of callus extracts was the highest at a clear zone of 16 mm.

Selective Detection of Campylobacter jejuni, C. coli, Arcobacter butzleri and Helicobacter pylori by Polymerase Chain Reaction (Campylobacter jejuni, C. coli, Arcobacter butzleri와 Helicobacter pylori의 PCR에 의한 분리검출)

  • Lee, Young-Duck;Park, Jong-Hyun
    • Korean Journal of Food Science and Technology
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    • v.34 no.6
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    • pp.1134-1139
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    • 2002
  • Campylobacter, Arcobacter, and Helicobacter, classified into the same rRNA superfamily VI by taxonomy, cause food-borne diseases, stomach ulcer, and gastric cancer. To detect each strain selectively from contaminated foods, PCR, multiplex-PCR, and restricion fragment length polymorphism (RFLP) were applied on Campylobacter, Arcobacter, and Helicobacter. The same PCR products could be detected using CHA primer targeted for 16S rRNA of Campylobacter, Arcobacter, and Helicobacter. To detect C. jejuni and C. coli from A. butzleri and H. pylori, pg50/pg3 primer targeted for fla A gene was used, and for A. butzleri, Arco2/Butz primer targeted for 23S rRNA was utilized. For H. pylori detection, icd1/icd2 primer targeted for isocitrate dehydrogenase gene was employed, and JEJ1/JEJ2 primer targeted for ceuE gene was effective for C. jejuni detection from the three strains. C. jejuni, C. coli could be separated from A. butzleri and H. pylori through PCR-RFLP using restriction enzyme Dde I. Such primers would be effective for detecting each strain selectively through PCR when C. jejuni, C. coli, A butzleri and H. pylori are contaminated together.

Omeprazole Based Antibiotic Regimens for Helicobacter pylori Infection in Peptic Ulcer Disease (Helicobacter pylori 감염 소화성궤양에서 Omeprazole중심 항생요법)

  • 강현주;강동훈;유종현;이숙향
    • YAKHAK HOEJI
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    • v.44 no.1
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    • pp.16-21
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    • 2000
  • Peptic ulcer is involved with Helicobacter pylori infection and antibiotic regimens are primary treatments. An optimal therapeutic regimen for eradication of Helicobacter pylori remains uncertain due to variable efficacy. The objectives of this study were to evaluate the efficacy of omeprazole based antibiotic regimens in bacterial eradication, healing of peptic ulcer and to identify factors affecting efficacy. Seventy-seven patients were enrolled in the prospective, open-trial from November 1997 to Setember 1998. H. pylori infection was identified with endoscopy, H. pylori stain and rapid urease test. The first group (OAC7) received omeprazole 20 mg twice daily for 4 weeks which were the same schedule for all, amoxicillin and clarithromycin 500 mg three times daily for 1 week; the second group (OAC14), for 2 weeks on the same regimen as the first; and the last group (OACD) has taken bismuth in addition to the OAC7 regimen for 1 week. Eradication of H. pylori and healing of peptic ulcer were evaluated with endoscopy and tests for H. pylori before and after treatments. There were no significant differences in eradication rates; 77% in OAC7, 76% in OAC14, 81% in OACD (p=0.935) and healing rates; 82% in OAC7, 71% in OAC14, 95% in OACD (p=0.179), respectively. Compliance had an relationship with eradication rates significantly among regimens (p=0.049). Twenty three cases (29%) complained of the minor side effects. In conclusion, OAC7 was better in convenience of dosing schedule and showed fewer side effects with shorter duration and lower cost while There were no significant differences in efficacy among regimens.

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