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RISS 인기검색어
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- 저자 : Bie Wei (검색결과 4 건)
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Frequency Hopping CR MAC Protocol in Cognitive Radio Ad Hoc Network
Mei Bie,Zhe Wang,Wei Xiao,Kai Song 보안공학연구지원센터 2015 International Journal of Multimedia and Ubiquitous Vol.10 No.9
To insure the fairness for the Cognitive Radio (CR) nodes with various available channels, a frequency hopping CR MAC protocol based dynamic (named DCR-MAC) is proposed. In the case of uneven distribution of frequency spectrum in cognitive Ad Hoc network, based on the numbers of workable channels of each cognitive node, DCR-MAC protocol adjusts access time dynamically, ensuring the node priority access channel number, in order to improve the overall performance of the network. Meanwhile, against the problem of the multi-channel hidden terminal which appears in cognitive network of single wireless interface configuration, through introducing the "data segment" mechanism, and informing present channels occupied condition of adjacent node via receiving node, DCR-MAC protocol broadcast of channel occupation in transmission channel, and prohibit possible data transmission of adjacent node, in order to solve this problem on this account. Finally, proving that DCR-MAC protocol is obviously excelled other FH CR MAC protocols in through put capacity, packet access delay, accessing fairness which through network simulation.
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송선범,장소영,강현태,Bie Wei,전운우,윤계순,황은성 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.7
Nicotinamide (NAM) plays essential roles in physiology through facilitating NAD+ redox homeostasis. Importantly, at high doses, it protects cells under oxidative stresses, and has shown therapeutic effectiveness in a variety of disease conditions. In our previous studies, NAM lowered reactive oxygen species (ROS) levels and extended cellular life span in primary human cells. In the treated cells, levels of NAD+/NADH and SIRT1 activity increased, while mitochondrial content decreased through autophagy activation. The remaining mitochondria were marked with low superoxide levels and high membrane potentials (Δψm); we posited that the treatment of NAM induced an activation of mitophagy that is selective for depolarized mitochondria, which produce high levels of ROS. However, evidence for the selective mitophagy that is mediated by SIRT1 has never been provided. This study sought to explain the mechanisms by which NAM lowers ROS levels and increases Δψm. Our results showed that NAM and SIRT1 activation exert quite different effects on mitochondrial physiology. Furthermore, the changes in ROS and Δψm were not found to be mediated through autophagy or SIRT activation. Rather, NAM suppressed superoxide generation via a direct reduction of electron transport, and increased Δψm via suppression of mitochondrial permeability transition pore formation. Our results dissected the effects of cellular NAD+ redox modulation, and emphasized the importance of the NAD+/NADH ratio in the mitochondria as well as the cytosol in maintaining mitochondrial quality.
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Yizhen Yu,Bingzhi Li,Yinsha Wei,Xinyue Ren,Fengsai Bie,Yang Xu,Ri Qiu,Xiaoguang Li,Yibo Ouyang 한국공업화학회 2023 Journal of Industrial and Engineering Chemistry Vol.118 No.-
In the harsh environment, the corrosion of Cu leads to the failure of pipelines, condenser, printed circuitboard and so forth. Thus, protecting Cu from corrosion is critically important from both science and engineeringbackgrounds. In this report, the hierarchical structure compositing dendritic Cu and ZIF-67 is preparedonto Cu by a two-step electrodeposition protocol. After thiol modification and oil infusion, bioinspiredsuperhydrophobic surface (SHS) and slippery liquid-infused porous surface (SLIPS) is respectivelyachieved, and sophisticated techniques are used for characterizing chemical composition, morphology,topology and wettability. Scanning Kelvin probe is employed to know the surface potentialdistribution before and after the biomimetic transformation. Using different electrochemical approaches,the corrosion inhibition effect is elucidated. In 3.5 wt% NaCl corrosive medium, |Z|0.01Hz of SLIPS is as highas 1.35 108 Xcm2 at the initial immersion stage. The value is remarkably enhanced compared with SHS(6.76 104 Xcm2) and bare Cu (8.74 103 Xcm2). After soaking for 168 h, |Z|0.01Hz value of SHS andSLIPS is 3.84 104 Xcm2 and 4.93 106 Xcm2, illustrating that SLIPS has high resistance to protectCu from corrosion.
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Song, Seon Beom,Jang, So-Young,Kang, Hyun Tae,Wei, Bie,Jeoun, Un-woo,Yoon, Gye Soon,Hwang, Eun Seong Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.7
Nicotinamide (NAM) plays essential roles in physiology through facilitating $NAD^+$ redox homeostasis. Importantly, at high doses, it protects cells under oxidative stresses, and has shown therapeutic effectiveness in a variety of disease conditions. In our previous studies, NAM lowered reactive oxygen species (ROS) levels and extended cellular life span in primary human cells. In the treated cells, levels of $NAD^+/NADH$ and SIRT1 activity increased, while mitochondrial content decreased through autophagy activation. The remaining mitochondria were marked with low superoxide levels and high membrane potentials (${\Delta}_{{\Psi}m}$); we posited that the treatment of NAM induced an activation of mitophagy that is selective for depolarized mitochondria, which produce high levels of ROS. However, evidence for the selective mitophagy that is mediated by SIRT1 has never been provided. This study sought to explain the mechanisms by which NAM lowers ROS levels and increases ${\Delta}_{{\Psi}m}$. Our results showed that NAM and SIRT1 activation exert quite different effects on mitochondrial physiology. Furthermore, the changes in ROS and ${\Delta}_{{\Psi}m}$ were not found to be mediated through autophagy or SIRT activation. Rather, NAM suppressed superoxide generation via a direct reduction of electron transport, and increased ${\Delta}_{{\Psi}m}$ via suppression of mitochondrial permeability transition pore formation. Our results dissected the effects of cellular $NAD^+$ redox modulation, and emphasized the importance of the $NAD^+/NADH$ ratio in the mitochondria as well as the cytosol in maintaining mitochondrial quality.
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