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유문간(Mun-Gan Rhyu),김진(Jin Kim),이원철(Won Chul Lee),주천기(Choun-Ki Joo),박조현(Cho-Hyun Park),권오주(Oh-Joo Kwon),김명석(Myung-Suk Kim) 한국의학교육학회 1999 Korean journal of medical education Vol.11 No.2
Over the past years, university administrators have known how hard it is to transform into the modern university. Rigid in-bred research system, narrow interest, unworkable graduate programs are complicatedly woven into a network of academic fraction. Cronyism and protectionism flood various laboratories and research institutes affiliated with the university. Until recently, the department structure of medical school has steadfastly guarded its territory and refused to allow non-medical undergraduate students to apply for the graduate schools of medical science. The graduate schools in medical science are considered just extra appendages because most of graduate students should be engaged in hard work position such as junior faculty or residentship training course of university hospital. In the present environment of graduate program, medical schools are consequently not able to bring in full-time young researchers, but only recently has its door been open for others. It should be time to reorganize the medical school graduate course into large multidisciplinary research group by expanding graduate programs.
한국형 출혈열 및 만성간염과 조직적합성 항원간의 유전적 관련성에 관한 연구 (Ⅱ) : (Ⅱ)만성간염과 조직적합성 항원간의 유전적 관련성에 관한 연구
한훈(Hoon Han),김태규(Tae-Kyu Kim),유문간(Moon-Gun Rhyu),임병욱(Byung-Uk Lim),김금용(Gum-Ryong Kim),이종훈(Chong-Hoon Lee),김부성(Boo-Sung Kim),김호연(Ho-Youn Kim),윤영석(Young-Suk Yoon),방병기(Byung-Kee Bang),민병석(Byong-Sok Min) 大韓微生物學會 1986 大韓微生物學會誌 Vol.21 No.2
Gastric Mucosal Atrophy Impedes Housekeeping Gene Methylation in Gastric Cancer Patients
오정환,유문간,김석일,윤미리,신정하,홍승진 대한암학회 2019 Cancer Research and Treatment Vol.51 No.1
Purpose Helicobacter pylori infection induces phenotype-stabilizing methylation and promotes gastric mucosal atrophy that can inhibit CpG-island methylation. Relationship between the progression of gastric mucosal atrophy and the initiation of CpG-island methylation was analyzed to delineate epigenetic period for neoplastic transformation. Materials and Methods Normal-appearing gastric mucosa was biopsied from 110 H. pylori–positive controls, 95 H. pylori–negative controls, 99 gastric cancer patients, and 118 gastric dysplasia patients. Gastric atrophy was assessed using endoscopic-atrophic-border score. Methylation-variable sites of eight CpG-island genes adjacent to Alu (CDH1, ARRDC4, PPARG, and TRAPPC2L) or LTR (MMP2, CDKN2A, RUNX2, and RUNX3) retroelements and stomach-specific TFF3 gene were analyzed using radioisotope-labeled methylation-specific polymerase chain reaction. Results Mean ages of H. pylori–positive controls with mild, moderate, and severe atrophy were 51, 54, and 65 years and those of H. pylori–associated TFF3 overmethylation at the three atrophic levels (51, 58, and 63 years) tended to be periodic. Alu-adjacent overmethylation (50 years) was earlier than TFF3 overmethylation (58 years) in H. pylori–positive controls with moderate atrophy. Cancer patients with moderate atrophy showed late Alu-adjacent (58 years) overmethylation and frequent LTR-adjacent overmethylation. LTR-adjacent overmethylation was frequent in cancer (66 years) and dysplasia (68 years) patients with severe atrophy. Conclusion Atrophic progression is associated with gastric cancer at moderate level by impeding the initiation of Alu-adjacent methylation. LTR-adjacent methylation is increased in cancer patients and subsequently in dysplasia patients.