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Kim, Sun Hong,Seo, Hyunseon,Kang, Jiheong,Hong, Jaeyoung,Seong, Duhwan,Kim, Han-Jin,Kim, Jaemin,Mun, Jaewan,Youn, Inchan,Kim, Jinseok,Kim, Yu-Chan,Seok, Hyun-Kwang,Lee, Changhee,Tok, Jeffrey B.-H.,Bao American Chemical Society 2019 ACS NANO Vol.13 No.6
<P>Both self-healable conductors and stretchable conductors have been previously reported. However, it is still difficult to simultaneously achieve high stretchability, high conductivity, and self-healability. Here, we observed an intriguing phenomenon, termed ?electrical self-boosting?, which enables reconstructing of electrically percolative pathways in an ultrastretchable and self-healable nanocomposite conductor (over 1700% strain). The autonomously reconstructed percolative pathways were directly verified by using microcomputed tomography and <I>in situ</I> scanning electron microscopy. The encapsulated nanocomposite conductor shows exceptional conductivity (average value: 2578 S cm<SUP>?1</SUP>; highest value: 3086 S cm<SUP>?1</SUP>) at 3500% tensile strain by virtue of efficient strain energy dissipation of the self-healing polymer and self-alignment and rearrangement of silver flakes surrounded by spontaneously formed silver nanoparticles and their self-assembly in the strained self-healing polymer matrix. In addition, the conductor maintains high conductivity and stretchability even after recovered from a complete cut. Besides, a design of double-layered conductor enabled by the self-bonding assembly allowed a conducting interface to be located on the neutral mechanical plane, showing extremely durable operations in a cyclic stretching test. Finally, we successfully demonstrated that electromyogram signals can be monitored by our self-healable interconnects. Such information was transmitted to a prosthetic robot to control various hand motions for robust interactive human-robot interfaces.</P> [FIG OMISSION]</BR>
단백질 검출을 위한 microcantilever 바이오센서의 제작과 응용
김준혁(Jun-Hyuk Kim),유경아(Kyung-Ah Yoo),정승룡(Seung-Ryong Joung),김한수(Han-Soo Kim),김재완(Jaewan Kim),최영진(Y. J. Choi),강치중(C. J. Kang),김용상(Yong-Sang Kim) 대한전기학회 2006 대한전기학회 학술대회 논문집 Vol.2006 No.7
화학적, 생물학적 분석, 즉 특정 물질의 존재 유무를 측정하기 위해 마이크로캔틸레버라는 구조체를 제작하여 이를 바이오센서로 응용하였다. 마이크로캔틸레버의 장점은 분석하고자 하는 시료의 양이 적더라도 감지가 가능하고 이를 통하여 분석시간을 단축할 수 있다는 장점을 가지고 있다. 마이크로캔틸레버 구조물 제작을 위해 보편적으로 많이 이용되는 bulk 미세 가공 기술을 대신하여 표면 미세 가공기술을 이용하였다. 이러한 표면 미세 가공기술은 bulk 미세 가공기술에 비해 공정이 간단하고 값이 싸다는 장점이 있다. 또 액상 실험을 위하여 polydimethylsiloxane (PDMS) 와 fused silica glass를 사용한 유제 제어 시스템을 제작하였다. 본 연구에서는 자기조립 이라는 특성을 이용하여 생물분자를 유체 제어 시스템 내의 마이크로캔틸레버 상단에 immobilization 시킨 후 마이크로캔틸레버 상, 하단의 표면 스트레스 차이에 따른 마이크로캔틸레버 자체의 휘어지는 정도를 측정하였다. 이러한 휘어지는 현상을 관찰함으로서 마이크로캔틸레버의 바이오센서로 응용 가능성을 확인할 수 있었다.
NRBF2-mediated autophagy contributes to metabolite replenishment and radioresistance in glioblastoma
Kim Jeongha,Kang Hyunkoo,Son Beomseok,Kim Min-Jung,Kang JiHoon,Park Kang Hyun,Jeon Jaewan,Jo Sunmi,Kim Hae Yu,Youn HyeSook,Youn BuHyun 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Overcoming therapeutic resistance in glioblastoma (GBM) is an essential strategy for improving cancer therapy. However, cancer cells possess various evasion mechanisms, such as metabolic reprogramming, which promote cell survival and limit therapy. The diverse metabolic fuel sources that are produced by autophagy provide tumors with metabolic plasticity and are known to induce drug or radioresistance in GBM. This study determined that autophagy, a common representative cell homeostasis mechanism, was upregulated upon treatment of GBM cells with ionizing radiation (IR). Nuclear receptor binding factor 2 (NRBF2)—a positive regulator of the autophagy initiation step—was found to be upregulated in a GBM orthotopic xenograft mouse model. Furthermore, ATP production and the oxygen consumption rate (OCR) increased upon activation of NRBF2-mediated autophagy. It was also discovered that changes in metabolic state were induced by alterations in metabolite levels caused by autophagy, thereby causing radioresistance. In addition, we found that lidoflazine—a vasodilator agent discovered through drug repositioning—significantly suppressed IR-induced migration, invasion, and proliferation by inhibiting NRBF2, resulting in a reduction in autophagic flux in both in vitro models and in vivo orthotopic xenograft mouse models. In summary, we propose that the upregulation of NRBF2 levels reprograms the metabolic state of GBM cells by activating autophagy, thus establishing NRBF2 as a potential therapeutic target for regulating radioresistance of GBM during radiotherapy.