http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
이경은 한국자료분석학회 2004 Journal of the Korean Data Analysis Society Vol.6 No.4
In this paper we consider the well-known Weibull regression models for survival analysis. These models are usually used with few covariates and many observations (subjects). But, for a typical setting of gene expression data from DNA microarray, we need to consider the case where the number of covariates exceeds the number of samples . For a given vector of response values which are times to event(death or censored times) and gene expressions(covariates), we address the issue of how to reduce the dimension by selecting the significant genes. This approach enables us to estimate the survival curve when . In our approach, rather than fixing the number of selected genes, we will assign a prior distribution to this number. The approach creates additional flexibility by allowing the imposition of constraints, such as bounding the dimension via a prior, which in effect works as a penalty. To implement our methodology, we use a Markov Chain Monte Carlo(MCMC) method. We demonstrate the use of the methodology to diffuse large B-cell lymphoma(DLBCL) complementary DNA(cDNA) data and Breast Carcinomas data.
NCTC-1469 생쥐 간세포주에 나타난 Acetaminophen 간독성
이경은 梨花女子大學校 醫科大學 醫科學硏究所 1998 EMJ (Ewha medical journal) Vol.21 No.4
Acetaminophen(AAP)은 임상적으로 자주 사용되는 해열·진통제로서 aspirin과 비교할 때 치료용량에서는 비교적 안전한 것으로 알려져 왔다. 그러나 과량 복용시에는 반응성과 산화성이 큰 중간대사물인 N-acetyl-p-benzoquinone imine에 의해 동물과 인간에서 심각한 간손상을 일으킨다고 한다. 일반적으로 세포죽음(cell death)은 세포괴사(necrosis)와 세포고사(apoptosis)의 두가지 기전을 통해 일어나며 최근 세포괴사와 세포고사는 모두 간세포 손상 기전에 관여할 것으로 여겨지고 있으나 이에 대한 연구가 미비한 실정이다. 이에 본 연구에서는 생쥐 간세포주인 NCTC clone 1469 세포주를 이용하여 AAP로 유도된 간독성 기전이 세포괴사인지 또는 세포고사인지를 검색하여 다음과 같은 결과를 얻었닫. NCTC-1469 세포주에서 24시간동안 AAP 투여시 농도 의존적으로 MTT 흡광도가 유의성있게 감소하였으며 lactate dehydrogenase유리는 AAP 농도에 의존적으로 증가하였다. 또한 LDH 유리와 간세포 생존율과의 상관관계에 대한 직선형 회귀분석을 시행하였을 때 매우 강한 역상관계를 나타내어 AAP투여는 NCTC-1468 세포주에서 세포괴사에 의한 세포 생존력 감소를 유발한다고 생각되었다. 한편 24시간 AAP 투여시 현저한 DNA 분절을 나타내었으나 농도에 대한 의존성을 나타내지 않았다. 따라서 acetaminophen 투여는 NCTC-1469 생쥐 간세포주에서 세포고사 및 세포괴사를 유도하며 주로 세포괴사에 의한 간세포 죽음을 야기하는 것으로 생각되었다. Acetaminophen is a mild analgesic and antipyretic agent that is safe and effective when taken in therapeutic doses. Ingestion of overdoses, however, may lead to acute liver failure accompanied by centrilobular degeneration and necrosis. The toxicity of acetaminophen is generally thought to be caused by direct interaction of its reactive metabolites with cellular macromolecules. Cell death, defined as an irreversible loss of vital cellular function and structure, can occur by either necrosis or apoptosis. Until recently, investigation into liver cell death has focused on cell necrosis although it is now appreciated that both apoptosis and necrosis may contribute to liver cell death. The present study examined cultured NCTC-1469 cells for LDH release and DNA laddering and their association with cell death. NCTC-1469 cells were cultured in NCTC-135 medium containing 10% horse serum for 72hr, and changed medium to fresh medium containing acetaminophen(from 0,5mM to 5mM). Cell viability was examined by MTT method and cell necrosis was assessed lactate dehydrogenase leakage. Genomic DNA fragmentation was assessed qualitatively by 1.5% agarose gel electrophoresis. Acetaminophen decreased MTT levels(p<0.05) and increased release of LDH(p<0.05) in dose-dependendent manner. Agarose gel electrophoresis revealed a "ladder" of DNA fragments in all acetaminophen concentration. Cell viability strongly correlated with cell necrosis(r^2=0.946). These results show that acetaminophen induced both necrosis and apoptosis in NCTC-1469 cells and cell death mainly attributed to apoptosis.