http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Yueh-Chun Li,Yi-Ju Pan,Fuu-Jen Tsai,Chyi-Chyang Lin 한국유전학회 2016 Genes & Genomics Vol.38 No.1
Partial 9p deletion syndrome and partial 18q duplication syndrome each have distinct clinical features. We describe the prenatal molecular cytogenetic analysis of a de novo unbalanced karyotype with deletion of 9p23-pter and duplication of 18q12.2-qter in a mild dysmorphic female fetus. Fetal ultrasonography was performed and detailed karyotype analyses were conducted using a combination of G-banding, SKY analysis and FISH with chromosome arm specific sub-telomeric DNA probes and chromosomal region specific BAC clone probes. The fetal sonography and fetal echocardiography at 17 weeks’ gestation did not reveal any anomaly while the fetus had a large unbalance karyotype of 46,XX,der(9)t(9;18) (p23;q12.2) de novo. Its external phenotype at 21 weeks appeared to have some mild dysmorphic features including hypertelorism, low-set ears, micrognathia/retrognathia, clenched hands and rocker bottom feet. These dysmorphic features are seen in the Edward syndrome but with milder degrees.
Chu-Chung Chou,Jai-Sing Yang,Hsu-Feng Lu,Siu-Wan Ip,Chyi Lo,Chih-Chung Wu,Jing-Pin Lin,Nou-Ying Tang,Jing-Gung Chung,Ming-Jen Chou,Ying-Hock Teng,Dar-Ren Chen 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.8
Dietary polyphenols have been correlated with a reduced risk of developing cancer. Quercetin (a natural polyphenolic compound) induced apoptosis in many human cancer cell lines, including breast cancer MCF-7 cells. However, the involvement of possible signaling pathways and the roles of quercetin in apoptosis are still undefined. The purpose of this study was to investigate the effects of quercetin on the induction of the apoptotic pathway in human breast cancer MCF-7 cells. When MCF-7 cells were treated with quercetin for 24 and 48 h and at various doses (10-175 μM), cell viability decreased significantly in time- and dose-dependent manners. Exposure of MCF-7 cells to 10-175 μM quercetin resulted in an approximate 90.25% decrease in viable cells. To explicate the mechanism underlying the antiproliferative effect of quercetin, cell cycle distribution and apoptosis in MCF-7 cells was investigated after exposure to 150 μM quercetin for 6-48 h. Quercetin caused a remarkable increase in the number of S phase (14.56%to 61.35%) and sub-G1 phase cells (0.1% to 8.32%) in a dose- and time-dependent manner. Quercetin caused S phase arrest by decreasing the protein expression of CDK2, cyclins A and B while increasing the p53 and p57 proteins. Following incubation with quercetin for 48 h, MCF-7 cells showed apoptotic cell death by the decreased levels of Bcl-2 protein and ΔΨ m and increased activations of caspase-6, -8 and -9. Moreover, quercetin increased the AIF protein released from mitochondria to nuclei and the GADD153 protein translocation from endoplasmic reticulum to the nuclei. These data suggested that quercetin may induce apoptosis by direct activation of the caspase cascade through the mitochondrial pathway in MCF-7 cells.