PURPOSES: Climbing lanes on expressways managed by the Korea Expressway Corporation (KEC) have been hot potatoes due to conflicts between slow-moving vehicles such as trucks and other vehicles at the merging section as well as the less popularity with the slow-moving vehicles. In order to resolve such problems, KEC has altered existing climbing lanes to passing-type climbing lanes in 1999. The new type of climbing lanes showed an apparent improvement in mobility. For example, the speeds of vehicles using both climbing lane and other lanes improved a lot. However, there has been no clear evidence about improved safety. METHODS: This research effort was initiated to evaluate the safety of the new passing-type climbing lanes using the comparison-group(CG) method based on three-year-long traffic accident data sets before and after the change, respectively. RESULTS: The passing-type climbing lanes showed twice increased traffic accidents even though the traffic accidents on old type climbing lanes increased 1.1% during the same periods. In addition, in-depth study, the merging area of the passing-type climbing lanes was found out to be the weakest section where 43.8% traffic accidents out of total traffic accidents happened. It is noted that the merging area of the old type climbing showed only 25.0% traffic accidents. CONCLUSIONS : The new passing-type climbing lanes were found to be weak in terms of safety when compared with the old type climbing lanes. Especially, the merging area should be improved to reduce the risk of traffic conflicts between slow-moving vehicles and other vehicles.

Human papillomavirus (HPV) has been classified as one of the causing factors of head and neck squamous cell carcinoma (HNSCC). However, little is known about HPV-related carcinogenesis in HNSCC. The purpose o f this s tudy i s to characterize immortalized human oral keratinocyte (IHOK) transfected by HPV16 E6/E7, IHOK/hcdk4 (IHOK transfected by pLXRN-hcdk4) and IHOK/hcdk4/hTERT (IHOK transfected by pLPC-hTERT-hcdk4) to reconstitute HNSCC in vitro. Conclusively, we established a new immortalized cell lines, IHOK/hcdk4 and IHOK/hcdk4/hTERT, to understand multistep carcinogenic process of oncogenic HPV16 E6/E7 in HNSCC.

to malignant transformation. Oral leukoplakia is a common premalignant lesion in oral mucosa and the incidence of cancer progression into SCC has been reported to be 0~43%. The genetic alterations of oncogenes, tumor suppressor genes and DNA repair genes occur during carcinogenesis. In order to evaluate the role of epithelial cells in the early stage of carcinogenesis, we analyzed the alterations of genetic heterogeneity in epithelial cells of oral leukoplakia samples, using Laser capture microdissection(LCM). The incidence rate of microsatellite instability(MSI) and loss of heterozygosity(LOH) were analysed from the DNA of epithelial cells from 16 leukoplakia samples using adjacent fibroblasts as a normal control. In this study, LOH was found in epithelial cells of all 16 cases of leukoplakias while MSI has been observed in 3 cases. Interestingly, the fibroblasts showed LOH and MSI in some cases, which was confirmed by DNA sequencing. Taken together, this study showed that leukoplakia has multiple genetic alterations in fibroblasts as well as in epithelial cells, suggesting that interaction between epithelial cells and fibroblasts might be involved in the early step of carcinogenesis.

구강면평 세포의 종양화는 여러 단계의 발생 순서를 거치는 다단계 발생과정 (multistep carcinogenesis) 으로 이루어지며 구강백 반증 (Ol'al leukoplakia)은 구강암 진행단계에서 악성암종으로 이행하기 전단계의 전암병소로 알려져 있다 이러힌 구강백빈 증이 악성 암종으 로 진행하는 빈도는 상피 이형성의 여부에 따라 6 6~36%로 니타나는데 이렇게 정상 상피 세 포가 암세포로 변환히는 과정에서는 종양 유전.7-}. 종양 억제 유전자.ONA 수복 유전지- 등 여러 유전자에 대한 지속적인 변이의 축적 이 나타난다 본 연구애서는 구강암의 전암벙 소인 구강백반증 조직 에서 싱피와 섬유모세포의 유전자 변이 분석을 위해 레이저 포획 미 세절제법 (laser capture microdissection) 을 이 용하여 16여| 의 겁체 에서 상피세포와 성유모세포를 각각 채취하고 구강암과 구강백반증에서 유전자 변이 분석에 사용된 26쌍의 mlCI'Osatellite( MSl) 표지자를 선정하여 각각의 이 형접합성상실 (Loss of Hetel"Ozygosity‘ LOH) 과 현미부수체 불안정성(Microsatellite in stability. MSI)을 분석 하였다. 연구 결과 구강 백반증 조직의 상피와 섬유모세포 모두에 LOH/MSI 가 발현함을 확인하였다 구강백반증 전체 조직에 서 LOH가 많이 나타나는 유전자의 위치는 염색체 21qll.l-21.1. 9p21-22. 3pI4-25. 17p12-14였고. MSI는 17p12-14‘ 5q21-23, 10q22-23 부위에서 많이 나타났으며 LOH는 섬유모세포 보다 상피세포에서. MSI는 상피세포 보다 섬유모세포에서 상대적으로 많이 발현하였다 상피이형 성이 있는 구강백반증을 그렇지 않은 경우와 비교하였을 때 06S264 표지자에서만 특이적으로 상피이형성이 있는 검체에서 LOH가 니티 났으며 나머지 표지자에서는 상피이형성괴 LOH 딸현 사이에 통계학적인 유의성이 없었다