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Step Up Therapy for Ulcerative Colitis, But Step Down Therapy for the Prevention of Colitic Cancer
Ki-Baik Hahm,Sang Woon Park,So Soon Kim,Hyun Sik Chung,Eun Jeong Jang,Jeong Sang Lee,Young-Joon Surh,Bong Hwan Kim,Seung Hee You,Hyun-Wook Baik,Sang Jong Park,Ju Sang Park,Wee Sik Son 大韓藥學會 2008 大韓藥學會 總會 및 學術大會 Vol.2008 No.2
Histologic Study of Chronic Active Hepatitis C: Comparison with Chronic Active Hepatitis B
Ki Baik Hahm,Chae Yoon Chon,Won Ho Kim,Kwang Hyub Han,Jae Bock Chung,Sang In Lee,Young Myung Moon,Jin Kyung Kang,In Suh Park,Heung Jai Choi,Eun Kyung Han,Chan Il Park 대한내과학회 1992 The Korean Journal of Internal Medicine Vol.7 No.2
Hahm, Ki Baik,Song, Young Joon,Oh, Tae Young,Lee, Jeong Sang,Surh, Young-Joon,Kim Young Bae,Yoo, Byung Moo,Kim, Jin Hong,Han, Sang Uk,Nahm, Ki Taik,Kim, Myung-Wook,Kim, Dae Yong,Cho, Sung Won 한국생화학분자생물학회 2003 BMB Reports Vol.36 No.1
Although debates still exist whether Helicobacter pylory infection is really class I carcinigen or not, H. pylori has been known to provoke precancerous lesions like gastric adenoma and chronic atrophic gastritis with intestinal metaplasia as well as gastric cancer, Chronic persistent, uncontrolled gastric inflammations are possible basis for ensuing gastric carcinogenesis and H. pylori infection increase COX-2 expressions, which might be the one of the mechanisms leading to gastric cancer. To know the implication of long-term treatment of antiinflammatory drugs, rebamipide or nimesulide, on H. pylori-associated gastric carcinogenesis, we infected C57BL/6 mice with H. pylori, expecially after MNU administration to promote carcinogenesis and the effects of the long-term administration of rebamipide or nimesulide were eva,uated. C57BL/6 mice werre sacrificed 50 weeks after H. pylori infection. Colonization rates of H.pylory, degree of gastric inflammation and other pathological changes including atrophic gastitis and metaplasia, serum levels and mRNA transcripts of various mouse cytoknes and chemokines, and NF-κ]B binding activities, and finally the presence of gastric adenocarcinoma were compared between H. pylori infected group (HP), and H.pylori infected group administrated with long-term rebamipide containing pellet diets (HPR) or nimesulide mixed pellets (HPN). Gastric mucosal expressions of ICAM-1, HCAM, MMP, and transcriptional regulations of Nf-κB binding were all significantly decreased in HPR group than in HP group. Multi-probe RNase protection assay showed the significantly decreased mRNA levels of apoptosis related genes and various cytokines genes like IFN-r, RANTES, TNF-α, TNFR p75, IL-1β in HPR group. In the experiment designed to provoke gastric cancer through MNU treatment with H.pylori infection, the incidence of gastric carcinoma was not changed between HP and HPR group, but significantly decreased in HPN group, suggesting the chemoprevention of H. pylori-associated gastric carcinogenesis by COX-2 inhibition. Long-term administration of antiinfalmmatory drugs should be considered in the treatment of H. pylori since they showed the molecular and biologic advantages with possible chemopreventive effect against H. pylori-associated gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis could be obtained, that will shed new light on chemoprevention of gastirc cancer, that is, that gastric cancer could be prevented through either the eradication of H. pylori or lessening the inflammation provoked by H. pylori infection in high risk group.
Hahm, Ki-Baik,Song, Young-Joon,Oh, Tae-Young,Lee, Jeong-Sang,Surh, Young-Joon,Kim, Young-Bae,Yoo, Byung-Moo,Kim, Jin-Hong,Ha, Sang-Uk,Nahm, Ki-Taik,Kim, Myung-Wook,Kim, Dae-Yong,Cho, Sung-Won Korean Society for Biochemistry and Molecular Biol 2003 Journal of biochemistry and molecular biology Vol.36 No.1
Although debates still exist whether Helicobacter pylori infection is really class I carcinogen or not, H. pylori has been known to provoke precancerous lesions like gastric adenoma and chronic atrophic gastritis with intestinal metaplasia as well as gastric cancer. Chronic persistent, uncontrolled gastric inflammations are possible basis for ensuing gastric carcinogenesis and H. pylori infection increased COX-2 expressions, which might be the one of the mechanisms leading to gastric cancer. To know the implication of long-term treatment of antiinflammatory drugs, rebamipide or nimesulide, on H. pylori-associated gastric carcinogenesis, we infected C57BL/6 mice with H. pylori, especially after MNU administration to promote carcinogenesis and the effects of the long-term administration of rebamipide or nimesulide were evaluated. C57BL/6 mice were sacrificed 50 weeks after H. pylori infection. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels and mRNA transcripts of various mouse cytokines and chemokines, and NF-${\kappa}B$ binding activities, and finally the presence of gastric adenocarcinoma were compared between H. pylori infected group (HP), and H. pylori infected group administered with long-term rebamipide containing pellet diets (HPR) or nimesulide mixed pellets (HPN). Gastric mucosal expressions of ICAM-1, HCAM, MMP, and transcriptional regulations of NF-${\kappa}B$ binding were all significantly decreased in HPR group than in HP group. Multi-probe RNase protection assay showed the significantly decreased mRNA levels of apoptosis related genes and various cytokines genes like IFN-$\gamma$, RANTES, TNF-$\alpha$, TNFR p75, IL-$1{\beta}$ in HPR group. In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not changed between HP and HPR group, but significantly decreased in HPN group, suggesting the chemoprevention of H. pylori-associated gastric carcinogenesis by COX-2 inhibition. Long-term administration of antiinflammatory drugs should be considered in the treatment of H. pylori since they showed the molecular and biologic advantages with possible chemopreventive effect against H. pylori-associated gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis could be obtained, that will shed new light on chemoprevention of gastric cancer, that is, that gastric/cancer could be prevented through either the eradication of H. pylori or lessening the inflammation provoked by H. pylori infection in high risk group.