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Insulin-like growth factor system : 흰쥐 턱밑샘에서의 증령적 mRNA 정량
류숙경,임채웅,김효분,손현진,조남표 대한구강악안면병리학회 2005 대한구강악안면병리학회지 Vol.29 No.5
Agi ng adversely affects the structure and function of the saliva ry gla nd and leads to ma rked insulin resis t ance that correlates with red uced ins ulin s ignal t ra nsduction, lnsulin-like g rowth factors are k.nown to be regulator involved in embryonic a nd postnatal development with sequences 62% identical t o that of proins ulin , To determine whether i n suli n- like growth facto l' - l, -2, - 1 receptor a l'e involved in the changes in rat salival'y gland by aging, we a na lyzecl the qua nti tation of 19f - 1, -2, - 1 rece ptor mRNA in l'at salivary glancl between 2 weeks and 26 months after bir th using the competiti ve reverse t ra nscriptase-polymerase chain reaction(RT-PCR) methocl Between 2 weeks ancl 2 months age, sharp falls in the qua nt ities of Igf-2 mRNA were observed, W11ereas Igf- 1 receptor mRNA rose by aging, but not sig nifïcantly, The quanti t ies of 19f- l kept by aging, These change seem to be involvecl a role fol' the Igf-2 in sali va ry c1evelopment a ncl earl y growth is incli ca ted, Thus, t he dras tic changes in the qua ntities of Igf-2 mRNA in the ra t sali va ry gla nd by aging seem to be in volved in the development, early growth and homeostasis of sali vary gla nd,
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CAI Courseware의 개발 : BASIC 언어를 중심으로
류숙경 ; 김혁진 김천대학교 1993 김천대학교 논문집 Vol.14 No.-
In this paper, We developed, adopted and analyzed CAl courseware for elementary school to learn BASIC language. The CAI courseware is make up of PRINT, LET, INPUT, and READ-DATA command in the present sixth grade textbook in elementary school, and there Learning Stage, Practice Stage, Usage Stage and Synthesis Stage in each stage. The CAl courseware used and developed Graphic, Animation and Sound for students to learn them interestingly. The CAI courseware analyzed the results of learning by means of a test and question paper to find out the student's accomplishment and response.
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김혁진 ; 류숙경 김천대학교 1994 김천대학교 논문집 Vol.15 No.-
In this thesis we analyze the part of addition and subtraction in the arithmetic texts of the first, second and third grades of Elementary Schools, taking their educational progress ystem into consideration. Then, we extract errors and mistakes of students' answers in the addition and subtraction ests and identify their error types through the personal interview. Such analytic method of error types are based on the experimental data. It can be a good help to find out their error types owing to the error classified code and to develop the each and learn software (CAI) which will support personal study drill efficiently in the future.
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구강 편평세포암종에서의 p16INK4A와 p15INK4B 발현과 메틸화의 관계
최철영,추정엽,류숙경,조남표 대한구강악안면병리학회 2003 대한구강악안면병리학회지 Vol.27 No.3
p16INK4A and p15INK4B tumor suppressor genes are frequently altered in various human tumors. Hypermethylation of the promoter region of p16INK4A and p15INK4B seem to be the major mechanism of inactivation. To determine whether the change in p16INK4A and p15INK4B methylation status occur in oral squamous cell carcinomas (OSCCs) and benign oral epithelial hyperplasias, we analyzed 46 OSCCs and 20 benign oral epithelial hyperplasias by methylation-specific PCR. We also analyzed a subset of the samples for p16INK4A and p15INK4B protein expression by immunohistochemistry. The promoter region of p15INK4B was hypermethylated in 13 specimens of the 15 finally analyzed OSCCs and three specimens of the five analyzed benign oral epithelial hyperplasias. By immunohistochemical analysis, we confirmed the loss of p15INK4B expression of all hypermethylated specimens. The promoter region of p16INK4A was amplified by both an unmethylated- and a methylated-specific primers in just one OSCCs. The remaining specimens including 11 OSCCs and four benign oral epithelial hyperplasias were normally methylated. By immunohistochemistry, we analyzed the loss of p16INK4A expression in seven specimens of the 12 OSCCs and two specimens of the four benign oral epithelial hyperplasias. Except for one OSCC, however, all specimens showing loss of expression were normally methylated. These results suggest that loss of p16INK4A and p15INK4B protein expression play an important role in the development of both OSCCs and benign oral epithelial hyperplasias.
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