http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Cho Rong Park,Chang Wook Jo,Kyu Sik Yoon,Min Ah Kang,Eun Jin Kang,Hye Ri Kwon,Mi Ja Seo,Yong Man Yu,Young Nam Youn 한국응용곤충학회 2009 한국응용곤충학회 학술대회논문집 Vol.2009 No.10
To identify DNA markers linked to a elytra polymorphism, amplified fragment length polymorphism (AFLP) analysis was performed on DNA samples from four each colour pattern individuals (2 females and males), for example, succinea 1, succinea 2, conspicua, and spectabilis. As a result of performing AFLP analysis with the restriction endonuclease combination EcoRⅠ and Mse I, total of 2,269 AFLP fragments which were specific to succinea, conspicua and spectabilis was identified using 24 different AFLP primer combinations. Among these 2,269 fragments, 16 bands which were the most specific to one color patterns were isolated, cloned and sequenced. Subsequent UPGMA cluster analysis revealed that population of H. axyridis was divided four major group and these genetic tree showed that H. axyridis elytra colour diversity was affected by genetic polymorphism. It is considered that these genetic analyses may be facilitated the understanding of molecular genetic mechanism related with the wing colour pattern formation in this species.
잉크젯 프린팅을 이용한 초박막 투명 TiO₂ 코팅층 제조
윤초롱(Cho-Rong Yoon),오효진(Hyo-Jin Oh),이남희(Nam-Hee Lee),Guo Yupeng,이원재(Won-Jae Lee),박경순(Kyeong-Soon Park),김선재(Sun-Jae Kim) 한국표면공학회 2007 한국표면공학회지 Vol.40 No.4
Dye sensitized solar cells(DSSC) are the most promising future energy resource due to their high energy efficiency, low production cost, and simple manufacturing process. But one problem in DSSC is short life time compared to silicon solar cells. This problem occurred from photocatalytic degradation of dye material by nanometer sized TiO₂ particles. To prevent dye degradation as well as to increase its life time, the transparent coating film is needed for UV blocking. In this study, we synthesized nanometer sized TiO₂ particles in sols by increasing its internal pressure up to 200 bar in autoclave at l20℃ for 10 hrs. The synthesized TiO₂ sols were all formed with brookite phase and their particle size was several ㎚ to 30 ㎚. Synthesized TiO₂ sols were coated on the backside of fluorine doped tin oxide(FTO) glass by ink jet printing method. With increasing coating thickness by repeated ink jet coating, the absorbance of UV region (under 400 ㎚) also increases reasonably. Decomposition test of titania powders dispersed in 0.1 mM amaranth solution covered with TiO₂ coating glass shows more stable dye properties under UV irradiation, compared to that with as-received FTO glass.
Yoon Kyong Ryu,Cho Rong Kim,Chi Won Kim,노태환,정옥상 대한화학회 2009 Bulletin of the Korean Chemical Society Vol.30 No.10
Ionic palladium(II) complex containing a long aliphatic chain, [(tmeda)PdL]2(PF6)4 (tmeda = N,N,N',N'-tetramethylethylenediamine;L = decylmethylbis(m-pyridyl)silane) allowed to form a puckered submicrosphere morphology without any template or additive. The puckered spheres reversibly adsorb and desorb dioxane molecules. Coligand and cosolvent effects on the formation of submicrospherical morphology were observed
Cho Rong Han(한초롱),Ji Young Lee(이지영),Dongki Kim(김동기),Hyo Young Kim(김효영),Se Jin Kim(김세진),Seokjoon Jang(장석준),Yoon Hee Kim(김윤희),Do Youn Jun(전도연),Young Ho Kim(김영호) 한국생명과학회 2013 생명과학회지 Vol.23 No.10
17α-estradiol (17α-E₂)의 에폽토시스 유도활성에 미치는 종양억제단백질 p53의 조절효과를 조사하고자, 17α-E₂에 의해 유도되는 에폽토시스 현상들을 인체 대장암 세포주 유래 클론인 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포에서 비교하였다. HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포를 17α-E₂ (2.5~10 μM)로 처리하거나 혹은 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포를 10 μM 17α-E₂로 시간 별로 처리한 결과, HCT116 (p53+/+)에 있어서는 세포독성과 에폽토시스-관련 sub-G₁ peak의 비율은 처리농도와 시간에 의존적으로 나타났다. 그러나 HCT116 (p53-/-) 세포의 경우는 이러한 현상이 미약하게 나타났다. 17α-E₂에 의해 유도되는 비정상적 유사분열방추사 형성, 중기판 염색체 배열의 미완성, 이에 따른 유사분열정지(G₂/M arrest) 등의 현상은 HCT116 (p53+/+) 및 HCT116 (p53-/-) 세포에서 유사한 수준으로 나타났다. 이에 반해, 17α-E₂에 의해 유도되는 Bak과 Bax의 활성화, 미토콘드리아의 막전위 상실(Δψm loss), 그리고 PARP 분해 등의 현상은 HCT116 (p53-/-) 세포에 비해 HCT116 (p53+/+) 세포에서 훨씬 높은 수준으로 확인되었다. 아울러 17α-E₂로 처리된 HCT116 (p53+/+) 세포에서 확인되는 p53 (Ser-15)의 인산화 및 p53 수준의 증가와 일치하여, 세포 내의 p21및 Bax 수준도 현저히 증가하였다. 이때 17α-E2로 처리된 HCT116 (p53-/-) 세포에서는 p21 및 Bax의 발현수준이 매우 낮았다. 한편, 에폽토시스 억제단백질인 Bcl-2 단백질수준은 HCT116 (p53-/-) 세포에 비해 HCT116 (p53+/+) 세포에서 다소 낮았으나, 이러한 Bcl-2 단백질 수준은 17α-E₂ 처리 후에도 크게 변화하지 않는 것으로 나타났다. 이러한 결과들은 17α-E₂ 처리에 의해 유도되는 에폽토시스 유도 경로의 구성원들의 변화, 즉 비정상적 유사분열방추사 형성 및 이에 따른 유사분열정지(G2/M arrest), 뒤이은 Bak 및 Bax의 활성화, 미토콘드리아의 막전위 상실, 그리고 이에 수반되는 caspase cascade 활성화 및 PARP 분해로 진행되는 에폽토시스 현상들 중에서, Bak 및 Bax의 활성화 단계가 종양억제단백질 p53의 에폽토시스 증진 활성에 의해 양성적으로 조절되는 작용 타켓임을 보여준다. The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of 17α-estradiol (17α-E₂) was compared between HCT116 (p53+/+) and HCT116 (p53-/-) cells. When the HCT116 (p53+/+) and HCT116 (p53-/-) cells were treated with 2.5~10 μM 17α-E₂ for 48 h or with 10 μM for various time periods, cytotoxicity and an apoptotic sub-G₁ peak were induced in the HCT116 (p53+/+) cells in a dose- and time-dependent manner. However, the HCT116 (p53-/-) cells were much less sensitive to the apoptotic effect of 17α-E₂. Although 17α-E₂ induced aberrant mitotic spindle organization and incomplete chromosome congregation at the equatorial plate, G₂/M arrest was induced to a similar extent in both cell types. In addition, 17α-E₂-induced activation of Bak and Bax, Δψm loss, and PARP degradation were more dominant in the HCT116 (p53+/+) than in the HCT116 (p53-/-) cells. In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 (p53+/+) cells treated with 17α-E₂. The HCT116 (p53-/-) cells exhibited barely or undetectable levels of p21 and Bax, regardless of 17α-E₂ treatment. On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 (p53+/+) than in the HCT116 (p53-/-) cells, it remained relatively constant after the 17α-E₂ treatment. Together, these results show that among the components of the 17α-E₂-induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, 17α-E₂-induced activation of Bak and Bax is the upstream target of proapoptotic action of p53.