• 제목/요약/키워드: HyeonMyeong Pyo

검색결과 22건 처리시간 0.016초

Au nano array formed on patterened $Al_2O_3$(0006)

  • 황재성;강현철;서옥균;오필건;이성표;이수용;김수남;김재명;조인화;노도영
    • 한국진공학회:학술대회논문집
    • /
    • 한국진공학회 2009년도 제38회 동계학술대회 초록집
    • /
    • pp.402-402
    • /
    • 2010
  • The formation of Au nano particles from thin films on patterned substrates depends sensitively on film thickness and time. The nano Au line and shape formed by annealing Au films on patterned oxide substrates are different from those formed on semiconductor. In this experiment, we deposited thin Au films on patterned $Al_2O_3$(0006) using E-beam evaporator, and annealed them at various temperatures and thickness under various conditions by RTA. We measured behavior of the Au during annealing Au structure and shape are changed when Au film becomes thicker. The shape of the resultant Au nano particles and their coarsening process are investigated using SEM and XRD.

  • PDF

Obesity Exacerbates Coxsackievirus Infection via Lipid-Induced Mitochondrial Reactive Oxygen Species Generation

  • Seong-Ryeol Kim;Jae-Hyoung Song;Jae-Hee Ahn;Myeong Seon Jeong;Yoon Mee Yang;Jaewon Cho;Jae-Hyeon Jeong;Younggil Cha;Kil-Nam Kim;Hong Pyo Kim;Sun-Young Chang;Hyun-Jeong Ko
    • IMMUNE NETWORK
    • /
    • 제22권2호
    • /
    • pp.19.1-19.20
    • /
    • 2022
  • Coxsackievirus B3 (CVB3) infection causes acute pancreatitis and myocarditis. However, its pathophysiological mechanism is unclear. Here, we investigated how lipid metabolism is associated with exacerbation of CVB3 pathology using high-fat diet (HFD)-induced obese mice. Mice were intraperitoneally inoculated with 1×106 pfu/mouse of CVB3 after being fed a control or HFD to induce obesity. Mice were treated with mitoquinone (MitoQ) to reduce the level of mitochondrial ROS (mtROS). In obese mice, lipotoxicity of white adipose tissue-induced inflammation caused increased replication of CVB3 and mortality. The coxsackievirus adenovirus receptor increased under obese conditions, facilitating CVB3 replication in vitro. However, lipid-treated cells with receptor-specific inhibitors did not reduce CVB3 replication. In addition, lipid treatment increased mitochondria-derived vesicle formation and the number of multivesicular bodies. Alternatively, we found that inhibition of lipid-induced mtROS decreased viral replication. Notably, HFD-fed mice were more susceptible to CVB3-induced mortality in association with increased levels of CVB3 replication in adipose tissue, which was ameliorated by administration of the mtROS inhibitor, MitoQ. These results suggest that mtROS inhibitors can be used as potential treatments for CVB3 infection.