• 보험의학회지
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• 제19권
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• pp.69-73
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• 2000

• 보험의학회지
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• 제19권
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• pp.9-14
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• 2000

• 한국축산식품학회:학술대회논문집
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• 한국축산식품학회 2001년도 정기총회 및 제27차 춘계학술발표회
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• pp.45-57
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• 2001

• Journal of Gastric Cancer
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• 제2권2호
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• Journal of Gastric Cancer
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• 제4권3호
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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.

• Asian Pacific Journal of Cancer Prevention
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• 제17권1호
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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.

• Journal of Preventive Medicine and Public Health
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• 제41권6호
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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.

• 생명과학회지
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• 제23권3호
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• pp.368-376
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• 2013

Helicobacter pylori 억제효과가 우수한 청목노상의 캘러스 배양을 위한 최적조건은 MS 고체배지에서 $27^{\circ}C$에서 20일간 배양하였을 때 6.4 mm의 크기로 가장 크게 자랐으며, 청목노상의 callus 형성에 미치는 생장조절제로는 NAA, 2,4-D, BA 및 kinetin 등을 2 mg/l의 농도로 첨가하여 $27^{\circ}C$에서 20일간 배양했을 때 높은 캘러스 성장률을 확인 할 수 있었고, 생장조절제의 혼합처리구가 단독처리구 보다 캘러스 형성율이 높은 것을 확인 할 수 있다. 따라서 본 연구에 사용된 청목노상 품종의 평판기내 배양을 위한 direct callogenesis의 최적 조건은 생장호르몬으로 2,4-D/NAA를 2 mg/l의 농도로 혼합 처리하여 $27^{\circ}C$에서 20일간 배양이 최적조건이었다. 청목노상 callus로부터 Helicobacter pylori 억제물질의 대량생산을 위한 방법인 biomass를 위한 bioreactor배양은 MS 액체배지에 호르몬으로 2,4-D와 BA를 각각 1 mg/l의 농도로 처리하여 20일간 배양하였을 때가 최적조건이었다. 최적조건에서 배양한 callus 추출물의 Helicobacter pylori 에 대한 억제효과는 16 mm의 clear zone으로 가장 높은 저해율을 확인할 수 있었다.

• 한국식품과학회지
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• 제34권6호
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• pp.1134-1139
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• 2002

Campylobacter, Arcobacter, Helicobacter는 분류학적으로 동일한 rRNA superfamily Ⅵ로 식중독 이외에도 위궤양, 위암, 유산 및 신경 장애를 유발한다. Campylobacter, Arcobacter, Helicobacter를 오염된 식품 등에서 선택적으로 검출하기 위해 PCR, multiplex-PCR, RFLP(restriction fragment length polymorphism)의 기법을 이용하였다. Campylobacter, Arcobacter, Helicobacter의 16S rRNA를 target으로 하는 CHA primer를 사용하여 동일한 PCR product의 검출할 수 있었다. C. jejuni와 C.coli를 A. butzleri와 H. pylori로부터 선택적으로 검출하기 위해 fla A gene을 target으로 하는 pg3, p50을 사용하였으며, A. butzleri는 23S rRNA를 target으로 하는 Arco2, Butz를 이용했다. 또한 H. pyloyi는 isocitrate dehydrogenase gene을 target으로 하는 icd1, icd2를 사용하였고, C. jejuni는 ceuE gene을 target으로 하는 JEJ1, JEJ2를 이용하여 효과적으로 분리검출이 이루어졌다. 또한 제한효소 Dde I 을 사용하여 PCR-RFLP를 통해 C. jejuni, C. coli를 A. butzleri, H. pylori로부터 분리할 수가 있었다. 따라서 이러한 primer를 이용하여 C. jejuni, C. coli, A. butzleri, H. pylori가 함께 오염되었을 때 각각 균주의 선택적인 검출이 가능할 것이다.

• 약학회지
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• 제44권1호
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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.