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( Hiun Suk Chae ),( Hyung Keun Kim ),( Jin Soo Kim ),( Hye Sook Son ),( Yong Wan Park ),( Eun Deuck Chang ),( Hye Kyung Lee ) 대한소화기학회 2007 SIDDS Vol.9 No.-
Background/Aims: Signaling pathways via ILK and beta-catenin are important ones in cancer progression and apoptosis of various cancer including colon and stomach. It roles of cancer cell are cell to adhesion, cell migration and motility. In colon cancer, two molecules are highly expressed. So we investigated their expression in colon polyps according to gross morphology and pathologic type. Methods: The expression of ILK and beta-catenin are measured with immunohistochemistry (Santa Cruz Co.) According to morphology, we calssified polyps into pedunculated polyps (Ip, 19), sessile polyps (Is, 31) and laterally spreading tumor (LST, 26). In pathologic type, colon polyps classified into adenocarcinoma (2), tubular adenoma (TA, 47), hyperplastic polyp (HP, 22), tubulovillous polyp (TV, 4), villous type (1). Results: According to morphology, there was no significant difference of ILK and beta-catenin expression among Ip, Is and LST (P>0.05). 2 malignant polyps revealed high expression of ILK and beta-catenin. ILK and beta-catenin expression in tubular adenomatous polyps were significantly higher than hyperplastic polyps (P<0.05). And in tubular adenoma, ILK and beta-catenin were highly expressed in high grade dysplasia (P<0.05). Conclusions: ILK and beta-catenin are not different in gross morphology of colon polyps but more expressed in tubular adenoma, especially in severe dysplasia.
Helicobacter pylori에 감염된 십이지장궤양과 비궤양성 소화불량에서 ABO 혈액형과 HLA의 연관
채현석(Hiun Suk Chae),김태규(Tai Gyu Kim),한훈(Hoon Han),김성수(Sung Soo Kim),최규용(Kyu Yong Choi),정인식(In Sik Chung),차상복(Sang Bok Cha),박두호(Doo Ho Park),김부성(Boo Sung Kim) 대한소화기학회 1996 대한소화기학회지 Vol.28 No.5
N/A Background/Aims: It has been known that genetic factors, for example, blood group, non-secretor and HLA system, are associated with duodenal ulcer and that Helicobacter pylori infection is the major cause of peptic ulcer. However, Helicobacter pylori is also found in non-ulcer dyspepsia and asyrnptomatic patients without ulcer formation. But, it is still not known regarding what kind of genetic factors have an effect on ulcer formation at the time of Helicobacter pylori infection. This study was performed to make clear wbich genetic factors are re1ated with duodenal ulcers among Koreans, and what kind of genetic factors could influence on the ulcer formation in the patients with Helicobacter pylori infection according to ABO blood groups and HLA antigen.'.. Methods: The duodenal ulcer patients (36), non-ulcer dyspepsia (19) and norraal healthy controls (103) were included in this study. Helicobacter pylori infection was detected with phenol red spray method in vivo which was confirmed with Warthin-Starry silver stain. HLA antigen expression (HLA-A,B) of peripheral blood T lymphocytes was studied with microlymphocytotoxicity teclmique. Results: Tbe frequency of HLA-A 33 was higher in duodenal ulcer patients (l4/36, 38.9%) compared with the control group (21/103, 20.4%). On the contrary, no difference in HLA-B has been shown between duodenal ulcer patients and controls. Among patients with Helicobacter pylori infection, blood group 0 was significant1y more frequent in patients with duodenal ulcers (21/36, 58.3%) than in non-ulcer dyspepsia (5/19, 26.3%). In patients with HLA-A 33, blood group 0 was significantly more frequent in duodenal ulcer patients (7/)4, 50%) than in non-ulcer dyspepsia patients (0/7, 0%). Conclusions: In Helicobacter pylori-infected patients, HLA-A 33 is related with duodenal ulcers and the patients with both blood group 0 and HI.A-A 33 are more likely to have duodeual ulcers than those with HLA-A 33 and without blood groop O. (Korean J Gastrnenterol 1996; 28:623 - 631)