|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Fabrication and characterization of 3D scaffold using 3D plotting system显示文摘In this paper, we design and fabricate a 3D scaffold using rapid prototyping (RP) technology for tissue engineering. The scaffold should have a three-dimensional interconnected pore network. We fabricate a polycaprolactone (PCL) scaffold with interconnecting pores and uniform porosity for cell ingrowth using a 3D plotting system. In order to keep the three dimensional shape under mechanical loading while implanted, we design an oscillating nozzle system to increase elastic modulus and yield strength of PCL strand. We characterize the influence of pore geometry, compressive modulus of the scaffold, elastic modulus and yield strength of the strand using SEM, dynamical mechanical analysis (DMA) and Nano-UTM. Finally the cell responses on scaffolds are observed. | LEE Jun-Hee PARK Su-A PARK KoEun KIM Jae-Hyun KIM Kyung-Shik LEE Jihye Kim WanDoo | 2010 | Chinese Science Bulletin2010，55，1： | 2 |
| 2 | An improved constitutive model for the numerical simulation of semi-solid thixofornaing显示文摘 | KOEUNE R PONTHOT J P | 2010 | Journal of Computational and Journal of Computational and Applied Mathematics2010，234，7： | 1 |
| 3 | Biosynthesis of capsinoid is controlled by the Pun1 locus in pepper显示文摘 | Koeun Han Hee-Jin Jeong Joohee Sung Young Soo Keum Myeong-Cheoul Cho Jeong-Han Kim Jin-Kyung Kwon Byung-Dong Kim Byoung-Cheorl Kang | 2013 | Molecular Breeding2013，，3： | 1 |
| 4 | Reactive oxygen species-induced activation of Yes-associated protein-1 through the c-Myc pathway is a therapeutic target in hepatocellular carcinoma显示文摘BACKGROUND The Hippo signaling pathway regulates organ size by regulating cell proliferation and apoptosis with terminal effectors including Yes-associated protein-1(YAP-1).Dysregulation in Hippo pathway has been proposed as one of the therapeutic targets in hepatocarcinogenesis.The levels of reactive oxygen species(ROS)increase during the progression from early to advanced hepatocellular carcinoma(HCC).AIM To study the activation of YAP-1 by ROS-induced damage in HCC and the involved signaling pathway.METHODS The expression of YAP-1 in HCC cells(Huh-7,HepG2,and SNU-761)was quantified using real-time polymerase chain reaction and immunoblotting.Human HCC cells were treated with H2O2,which is a major component of ROS in living organisms,and with either YAP-1 small interfering RNA(siRNA)or control siRNA.To investigate the role of YAP-1 in HCC cells under oxidative stress,MTS assays were performed.Immunoblotting was performed to evaluate the signaling pathway responsible for the activation of YAP-1.Eighty-eight surgically resected frozen HCC tissue samples and 88 nontumor liver tissue samples were used for gene expression analyses.RESULTS H2O2 treatment increased the mRNA and protein expression of YAP-1 in HCC cells(Huh-7,HepG2,and SNU-761).Suppression of YAP-1 using siRNA transfection resulted in a significant decrease in tumor proliferation during H2O2 treatment both in vitro and in vivo(both P<0.05).The oncogenic action of YAP-1 occurred via the activation of the c-Myc pathway,leading to the upregulation of components of the unfolded protein response(UPR),including 78-kDa glucoseregulated protein and activating transcription factor-6(ATF-6).The YAP-1 mRNA levels in human HCC tissues were upregulated by 2.6-fold compared with those in nontumor tissues(P<0.05)and were positively correlated with the ATF-6 Levels(Pearson’s coefficient=0.299;P<0.05).CONCLUSION This study shows a novel connection between YAP-1 and the UPR through the c-Myc pathway during oxidative stress in HCC.The ROS-induced activation of YAP-1 via the c-Myc pathway,which leads to the activation of the UPR pathway,might be a therapeutic target in HCC. | Yuri Cho Min Ji Park Koeun Kim Sun Woong Kim Wonjin Kim Sooyeon Oh Joo Ho Lee | 2020 | World Journal of Gastroenterology2020，26，42： | 1 |
| 5 | CRISPR/Cas9-mediated gene editing to confer turnip mosaic virus (TuMV) resistance in Chinese cabbage (Brassica rapa)显示文摘Genome editing approaches,particularly the CRISPR/Cas9 technology,are becoming state-of-the-art for trait development in numerous breeding programs.Significant advances in improving plant traits are enabled by this influential tool,especially for disease resistance,compared to traditional breeding.One of the potyviruses,the turnip mosaic virus(TuMV),is the most widespread and damaging virus that infects Brassica spp.worldwide.We generated the targeted mutation at the eIF(iso)4E gene in the TuMV-susceptible cultivar“Seoul”using CRISPR/Cas9 to develop TuMV-resistant Chinese cabbage.We detected several heritable indel mutations in the edited T0 plants and developed T1 through generational progression.It was indicated in the sequence analysis of the eIF(iso)4E-edited T1 plants that the mutations were transferred to succeeding generations.These edited T1 plants conferred resistance to TuMV.It was shown with ELISA analysis the lack of accumulation of viral particles.Furthermore,we found a strong negative correlation(r=-0.938)between TuMV resistance and the genome editing frequency of eIF(iso)4E.Consequently,it was revealed in this study that CRISPR/Cas9 technique can expedite the breeding process to improve traits in Chinese cabbage plants. | Ye-Rin Lee Muhammad Irfan Siddique Do-Sun Kim Eun Su Lee Koeun Han Sang-Gyu Kim Hye-Eun Lee | 2023 | Horticulture Research2023，10，6： | 0 |
| 6 | 辣椒Pun1位点对辣椒素酯类物质合成的控制显示文摘辣椒由于含有生物碱化合物辣椒素和辣椒素类物质(capsaicinoids)而具有独特的辣味。虽然辣椒素类物质已被证实对人体健康有药理和生理作用,但由于具有辛辣味,使得辣椒素类物质的应用受到限制。在无辣味的辣椒中发现的辣椒素酯类物质(capsinoids)与辣椒素类物质具有非常相近的结构和相似的生物效应。以前的研究表明,p-AMT基因突变与辣椒素酯类物质的产生相关,然而,辣椒素酯类物质的合成途径尚未被完全阐明。在本研究中,我们对F6重组自交系群体进行了遗传分析,以确定辣椒素酯类物质的合成机制。在这个群体中,辣椒素酯类物质的产生与否表现出了与具有Pun1位点的基因型植株的共分离。此外,我们筛选了辣椒素酯类物质的合成模式,以及在p-AMT突变系中Pun1位点与辣椒素酯类物质合成的相关性。在辣椒种质中,我们筛选到p-AMT基因中PLP结合结构域中的氨基酸取代突变体。隐性pun1基因存在时不合成辣椒素酯类物质,同时还发现p-AMT突变型和辣椒素酯类物质的含量之间并无关系。由此认为Pun1基因不仅负责辣椒素类物质合成,同时也控制着辣椒素酯类物质的合成。 | Koeun Han Hee-Jin Jeong Joohee Sung Young Soo Keum Myeong-Cheoul Cho Jeong-Han Kim Jin-Kyung Kwon Byung-Dong Kim Byoung-Cheorl Kang 孔秋生(译) | 2013 | 辣椒杂志2013，，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员