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주사 탐침 현미경을 이용하여 표면 처리한 기판 위의 DNA 관찰
이남주,손정민,진상협,전동렬,강치중 명지대학교 자연과학연구소 2004 자연과학논문집 Vol.23 No.-
대장균에서 추출한 plasmid DNA를 운모 기판에 착상시켜 주사 탐침 현미경으로 관찰하였다. plasmid DNA를 운모 기판에 착상시키기 위하여 운모 기판을 염 이온으로 0.01~10mM까지 농도를 변화시켜 표면 처리하였다. 운모 기판 위 염 이온의 농도 차이를 X-선 광전 분광기(XPS)로 표면을 분석하였다. 기판 처리에 사용한 염 이온의 농도에 영향을 받아 착상된 DNA의 밀도 및 모양이 변화하였다. 운모 기판 처리 농도에 따른 AFM 영상 차이와 XPS로 분석한 기판 위의 염 이온의 상태를 제시하고, 이들 사이의 상관관계에 대하여 논의하였다. The plasmid DNA on mica is observed using scanning probe microscopy. The mica surface is treated by 0.01~10mM NiCl_(2) for depositing the plasmid DNA. Concentration difference of NiCl_(2) on mica is analyzed a treated mica surface using XPS. The plasmid DNA on the treated mica has a difference of density and conformation in proportion as Ni^(2+) concentration. We present AFM topology difference and Ni^(2+) states on mica by XPS, discuss interaction between AFM topology difference and Ni^(2+) states on mica
쌍태아에서 제 1태아의 분만 후 제 2태아의 지연분만 : 중례보고
김주환,서민정,유희정,노권일,조대현,박정규,이정헌,조성남,손영수 朝鮮大學校 附設 醫學硏究所 2005 The Medical Journal of Chosun University Vol.30 No.3
With the widespread use of fertility medications and techniques of in vitro fertilization, multiple gestation has become epidemic in modern obstetric practice. Delivery of the initial fetus in a multiple gestation usually is followed by delivery of the subsequent fetus or fetuses shortly thereafter. However in rare circumstances, the delivery is delayed for days due to disappearance of uterine contraction after delivery of the first fetus. When uterine activity ceases after the delivery of the first neonate, a policy of nonintervention may be considered in case of an immature or very premature delivery, in order to achieve a gestational age for the remaining fetus(es) more compatible with neonatal survival. We report a case of twin gestation with prolongation of the delivery interval between the twins for 46 days.
Electrostatic Force Microscopy Plasmid DNA의 전기적 특성 관찰
이남주,손정민,진상협,전동렬,강치중 명지대학교 자연과학연구소 2004 자연과학논문집 Vol.23 No.-
p53HIS plasmid DNA를 운모 기판에 착상시켜 기판과 DNA 사이의 전기적인 특성을 electrostatic force microscope(EFM)와 atomic force microscope(AFM)을 이용하여 관찰하였다. DNA를 운모 기판 위에 착상시키기 위해 표면을 NiCl_(2) 용액으로 염 이온 처리했다. 염 이온의 농도에 따라 DNA와 기판과의 상호 작용에 의해 착상량과 DNA 단차 및 EFM 신호(DNA 외관상 단차)에 차이가 있었다. 즉, 염 농도가 높을수록 운모 기판에 고정되어 있는 DNA양이 많아졌고 기판과의 강한 상호 작용에 의해 DNA의 높이가 낮아지는 것을 관찰할 수 있었다. 반면 EFM신호는 탐침과 기판간의 척력 증가에 의해 증가하는 경향을 보였다. 또한 DNA의 한 부분에 전기적인 스트레스를 주었을 때의 특성을 EFM을 이용하여 분석하였다. We observe electrical characteristics between the plasmid DNA and mica by electrostatic force microscopy (EFM) and atomic force microscope (AFM). Firstly, we treated the mica by NiCl_(2) solution for depositing DNA. We monitored density of DNA molecules, DNA height and EFM signal from DNA-substrate interaction as Ni^(2+) concentration. We observe the plasmid DNA's height as Ni^(2+)concentration using AFM. On the other hand, EFM signal increase by increased repulsion between probe and substrate. After introducing voltage stress to a local area of DNA molecule, apparent height difference of DNA molecules was measured due to the charge injection or removal. Similar experiments were done with different bias polarities and sequential stress steps.
Surgical Outcomes of Adrenocortical Carcinoma; 20 Years of Experience in a Single Institution
Min Jhi Kim,Eun Jeong Ban,Soo Jung Jung,Hai Young Son1,Cho Rok Lee,Sang-Wook Kang,Jong Ju Jeong,Kee-Hyun Nam,Woong Youn Chung,Cheong Soo Park 대한갑상선-내분비외과학회 2014 The Koreran journal of Endocrine Surgery Vol.14 No.4
Purpose: Adrenocortical carcinoma (ACC) is a rare malignant tumor. Early detection is difficult and prognosis is poor. We report on 20 years of ACC surgical experience at our institution. Methods: This study included 32 ACC patients who underwent surgical resection at the Department of Surgery of the Yonsei University Health System in South Korea between January 1990 and February 2012. We reviewed these 32 patients and retrospectively analyzed long-term clinical outcomes and prognosis after radical surgery for ACC. Results: The median age of the 32 patients at diagnosis was 42.25 years (range 3∼81 years). There were 16 (50%) female and 16 (50%) male patients. Mean tumor size was 12.36 cm (range 1.8∼20 cm). Twenty-five patients (78.12%) had nonfunctioning tumors while the other seven patients (21.87%) had functioning tumors. Seventeen patients (53.12%) were classified as stage II, two (6.25%) as stage III, and 13 (40.62%) as stage IV. Fourteen patients underwent radical surgical resection, while 14 patients received adjuvant chemotherapy, two received adjuvant radiotherapy, and two received adjuvant chemoradiation. Four patients were lost to follow-up. Among the remaining 28 patients, 15 patients survived. The 5- and 10-year overall survival was 60.6% and 37.8%, respectively (median survival=85±24.3 months). Seventeen patients (53%) experienced disease recurrence. Five- and 10-year recurrence-free survival was 41.5% and 29.7%, respectively (median survival=18±5.5 months). Conclusion: Early stage at diagnosis and surgical resection were the most important prognostic factors associated with prolonged survival. The role of additional therapy remains controversial and new agents should continually be evaluated for efficacy.
Nam, Ju-Ock,Son, Hye-Nam,Jun, Eunsung,Cha, Kiweon,Lee, Byung-Heon,Park, Rang-Woon,Kim, In-San American Association for Cancer Research 2012 Molecular Cancer Research Vol.10 No.8
<P>It is known that VEGF receptors (VEGFR) and integrins interact with each other to regulate angiogenesis. We reported previously that the fasciclin 1 (FAS1) domain-containing protein, TGFBIp/beta ig-h3 (TGF-beta-induced protein) is an angiogenesis regulator that inhibits both endothelial cell migration and growth via alpha v beta 3 integrin. In an attempt to target the interaction between VEGFR-2 and alpha v beta 3 integrin, we determined whether the FAS1 domain region of TGFBIp/beta ig-h3 (FAS1 domain protein) can block the interaction between the two receptors, leading to the suppression of angiogenesis. In this study, we showed that FAS1 domain protein inhibits VEGF(165)-induced endothelial cell proliferation and migration via avb3 integrin, resulting in the inhibition of VEGF(165)-induced angiogenesis. We also defined a molecular mechanism by which FAS1 domain protein blocks the association between alpha v beta 3 integrin and VEGFR-2, showing that it binds to alpha v beta 3 integrin but not to VEGFR-2. Blocking the association of these major angiogenic receptors with FAS1 domain protein inhibits signaling pathways downstream of VEGFR-2. Collectively, our results indicate that FAS1 domain protein, in addition to its inhibitory effect on alpha v beta 3 integrin-mediated angiogenesis, also inhibits VEGF165-induced angiogenesis. Thus, FAS1 domain protein can be further developed into a potent anticancer drug that targets two principal angiogenic pathways. Mol Cancer Res; 10(8); 1010-20. (c) 2012 AACR.</P>
Exercise-Induced Vasospastic Angina With Prominent Regional Wall Motion Abnormality
Byeng-Ju Son,Jong-Il Park,Jong-Ho Nam,Chan-Hee Lee,Jang-Won Son,Ung Kim,Jong-Seon Park,Kang-Un Choi 아시아심장혈관영상의학회 2024 Cardiovascular Imaging Asia Vol.8 No.1
In vasospastic angina, exercise typically does not lead to vasoconstriction. We present the case of a patient with an atypical presentation of vasospastic angina, characterized by regional wall motion abnormalities confirmed by exercise stress echocardiography. A 58-year-old female patient presented to the hospital reporting chest pain during both exercise. During the exercise stress echocardiogram, regional wall motion abnormality was confirmed. However, the coronary angiography did not reveal significant lesions. Subsequently, ergonovine test was positive and then exercise induced vasospastic angina was diagnosed. Following medical treatment, the patient’s symptoms showed improvement. This case underscores an uncommon presentation of vasospastic angina in an individual already diagnosed with coronary artery disease, indicating that exercise stress echocardiography could serve as a valuable screening tool for specific types of vasospastic angina.
Son, Cheol-Hun,Keum, Jin-Hee,Yang, Kwangmo,Nam, Jiho,Kim, Mi-Ju,Kim, Sun-Hee,Kang, Chi-Dug,Oh, Sae-Ock,Kim, Chi-Dae,Park, You-Soo,Bae, Jaeho BioMed Central 2014 Radiation oncology Vol.9 No.-
<P><B>Background</B></P><P>The overexpression of histone deacetylase (HDAC) and a subsequent decrease in the acetylation levels of nuclear histones are frequently observed in cancer cells. Generally it was accepted that the deacetylation of histones suppressed expression of the attached genes. Therefore, it has been suggested that HDAC might contribute to the survival of cancer cells by altering the NKG2D ligands transcripts. By the way, the translational regulation of NKG2D ligands remaines unclear in cancer cells. It appears the modulation of this unclear mechanism could enhance NKG2D ligand expressions and the susceptibility of cancer cells to NK cells. Previously, it was reported that irradiation can increase the surface expressions of NKG2D ligands on several cancer cell types without increasing the levels of NKG2D ligand transcripts via ataxia telangiectasia mutated and ataxia telangiectasia and Rad3 related (ATM-ATR) pathway, and suggested that radiation therapy might be used to increase the translation of NKG2D ligands.</P><P><B>Methods</B></P><P>Two NSCLC cell lines, that is, A549 and NCI-H23 cells, were used to investigate the combined effects of ionizing radiation and HDAC inhibitors on the expressions of five NKG2D ligands. The mRNA expressions of the NKG2D ligands were quantitated by multiplex reverse transcription-PCR. Surface protein expressions were measured by flow cytometry, and the susceptibilities of cancer cells to NK cells were assayed by time-resolved fluorometry using the DELFIA® EuTDA cytotoxicity kit and by flow cytometry.</P><P><B>Results</B></P><P>The expressions of NKG2D ligands were found to be regulated at the transcription and translation levels. Ionizing radiation and HDAC inhibitors in combination synergistically increased the expressions of NKG2D ligands. Furthermore, treatment with ATM-ATR inhibitors efficiently blocked the increased translations of NKG2D ligands induced by ionizing radiation but did not block the increased ligand translations induced by HDAC inhibitors. The study confirms that increased NKG2D ligand levels by ionizing radiation and HDAC inhibitors could synergistically enhance the susceptibilities of cancer cells to NK-92 cells.</P><P><B>Conclusions</B></P><P>This study suggests that the expressions of NKG2D ligands are regulated in a complex manner at the multilevel of gene expression, and that their expressions can be induced by combinatorial treatments in lung cancer cells.</P>