http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Comet assay를 이용한 Ferric Sulfate의 유전자 독성에 대한 연구
박혜련,정태성,김신,강호승 大韓小兒齒科學會 2000 大韓小兒齒科學會誌 Vol.27 No.1
치수절단술은 유치의 치수치료 방법 중 사용빈도가 높은 시술 중 하나로 치수절단 술식에 사용되는 약제는 치수나 주위조직에 무해하여야 하며, 감염이나 내흡수 등의 부작용이 없어야 한다. 본 연구는 임상에서 유치의 지혈적 치수절단 술식의 약제로 사용되는 ferric sulfate의 유전자 독성을 평가할 목적으로 human gingival fibroblast에 ferric sulfate를 다양한 농도와 접촉시간을 설정한 후 comet assay를 이용하여 유전자 독성을 평가하여 보았다. 그 결과는 다음과 같다. 1. 농도에 따른 세포의 유전자 손상정도의 변화는 ferric sulfate의 농도에 비례하여 유전자 손상이 증가하는 양상을 나타내었다. 2. 농도에 따른 세포의 유전자 손상정도는 0.1,mM이상의 농도에서 대조군과 유의한 차이를 나타내었다.(p<0.05) 3. 시간경과에 따른 세포의 유전자 독성의 변화는 대조군과 유의한 차이를 보이지 않았다(P>0.05). Although ferric sulfate has been proposed as an alternative to formocresol in pulpotmy treatment in primary teeth, it has been given little concern regarding its cytotoxicity and mutagenicity. In the present study, we assessed the in vitro genotoxic effect of a ferric sulfate on human gingival fibroblast cell line (HGF-1), DNA damage was evaluated using comet assay (single cell alkaline gel electrophoresis) and obtained the results as follows: 1. A dose-response relationship was found between ferric sulfate concentrations (0 to 5mM)and DNA damages. 2. Above the concentration of 0.1mM, DNA damage was significantly increased than those of the control (p<0.05). 3. At the fixed concentration of 0.05mM, no significant difference was found between exposure time and DNA damage. These findings suggest that ferric sulfate as a pulpotomy agent can induce DNA damage in human gingival fibroblasts.
하악골에서 발생한 골아 세포종을 닮은 골육종의 치험 1례
이성근,정인교,박혜련 대한악안면성형재건외과학회 2000 Maxillofacial Plastic Reconstructive Surgery Vol.22 No.3
Typical osteoblastoma is generally considered to be a rare benign primary bone tumor that is seen primarily in children and young adults and curable by complete excision. However, the recurrence, aggressive behavior, or malignant transformation of this lesion was reported in some cases. It is reported that the malignant or aggressive osteoblatoma is really osteoblastoma-like osteosarcoma. Therefore, although this lesion is diagnosed as benign histologically. the operator must observe the postoperative course carefully. This article is to report a case of osteoblastoma-like osteosarcoma occurred in the mandible of 22 years old male patient with literature review.
Control of ASK1 Activity Via Protein-Protein Interaction
Hae Ryoun Park 대한구강악안면병리학회 2005 대한구강악안면병리학회지 Vol.29 No.5
ASKl(apoptosis signal-regulating kinase 1) is an important mediator of a poptotic s ignaling initi ated by a variety of death stimuli, including tumor necrosis factor ‘ Fas activat ion, oxidative st ress, and DNA damage. It was originally discovered as a mitogen -activated protein kinase kinase kinase(MAP3K) with proapoptotic activ ity Wben the A8Kl is stimulated, it activates both the MKK4/MKK7-JNK pathway and the M와(3/MKK6- p38 ki nase pathway‘ leading to stress responses or apoptosis. Owing to its critical role in promoting apoptosis. ASKl activity is highly control led in cells by multiple mechanisrns, includ ing phos ph이 ylation , oligomeri zation, and protein protein inte ractions. Phosphorylation of A8Kl at Thr-845 has been correlated with its acti vation . while phos phorylation at 8er-83 by Akt/protein kinase B attenuates A8Kl activity . It has also been demonst rated that in tramol ecular interaction, probably between the NH2• terminal and COOH-terminal domains of ASKl, may be required to maintain A8Kl in its inactive state, whereas oligomeri zation of its COOH- terminal domains is correlated with ASKl activation. The most commonly observed means of ASKl regulation, however, is thrO\땅h protein-protein in teractions. Numerous proteins have been shown to bind ASKl to exert theiJ‘ reg버atory function. For example. binding of TRAF2 0 1' Daxx promotes ASK1 funct ion, whereas the kinase and proapoptotic activities of A8Kl a re inhibited by many other associated proteins, including reduced t hi oredoxin, glutaredoxin, Cdc25A‘ Hsp 72, A8Kl - in teracting protein 1. and 14-3-3 proteins. A novel mechan ism of the anti-apoptotic action of Raf-l via phys ical interaction with ASKl wi ll be described. Furthermore, signifi cance of phosphorylati on s ite of 8er-1034 in the C-terminal regula tory domain of A8Klin the apoptotic activity wil l be discussed
Kang, Hae‐,Mi,Park, Bong‐,Soo,Kang, Hyun‐,Kyung,Park, Hae‐,Ryoun,Yu, Su‐,Bin,Kim, In‐,Ryoung John Wiley and Sons Inc. 2018 Environmental toxicology Vol.33 No.6
<P><B>Abstract</B></P><P>Delphinidin is major anthocyanidin that is extracted from many pigmented fruits and vegetables. This substance has anti‐oxidant, anti‐inflammatory, anti‐angiogenic, and anti‐cancer properties. In addition, delphinidin strongly suppresses the migration and invasion of various cancer cells during tumorigenesis. Although delphinidin has anti‐cancer effects, little is known about its functional roles in osteosarcoma (OS). For these reasons, we have demonstrated the effects of delphinidin on OS cell lines. The effects of delphinidin on cell viability and growth of OS cells were assessed using the MTT assay and colony formation assays. Hoechst staining indicated that the delphinidin‐treated OS cells were undergoing apoptosis. Flow cytometry, confocal microscopy, and a western blot analysis also indicated evidence of apoptosis. Inhibition of cell migration and invasion was found to be associated with epithelial‐to‐mesenchymal transition (EMT), observed by using a wound healing assay, an invasion assay, and a western blot analysis. Furthermore, delphinidin treatment resulted in a profound reduction of phosphorylated forms of ERK and p38. These findings demonstrate that delphinidin treatment suppressed EMT through the mitogen‐activated protein kinase (MAPK) signaling pathway in OS cell lines. Taken together, our results suggest that delphinidin strongly inhibits cell proliferation and induces apoptosis. Delphinidin treatment also suppresses cell migration and prevents EMT via the MAPK‐signaling pathway in OS cell lines. For these reasons, delphinidin has anti‐cancer effects and can suppress metastasis in OS cell lines, and it might be worth using as an OS therapeutic agent.</P>