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您的检索式：作者名="C.Armstrong"
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| 1 | EMP control and characterization on high-power laser systems显示文摘Giant electromagnetic pulses(EMP) generated during the interaction of high-power lasers with solid targets can seriously degrade electrical measurements and equipment. EMP emission is caused by the acceleration of hot electrons inside the target, which produce radiation across a wide band from DC to terahertz frequencies. Improved understanding and control of EMP is vital as we enter a new era of high repetition rate, high intensity lasers(e.g. the Extreme Light Infrastructure).We present recent data from the VULCAN laser facility that demonstrates how EMP can be readily and effectively reduced. Characterization of the EMP was achieved using B-dot and D-dot probes that took measurements for a range of different target and laser parameters. We demonstrate that target stalk geometry, material composition, geodesic path length and foil surface area can all play a significant role in the reduction of EMP. A combination of electromagnetic wave and 3 D particle-in-cell simulations is used to inform our conclusions about the effects of stalk geometry on EMP,providing an opportunity for comparison with existing charge separation models. | P.Bradford N.C.Woolsey G.G.Scott G.Liao H.Liu Y.Zhang B.Zhu C.Armstrong S.Astbury C.Brenner P.Brummitt F.Consoli I.East R.Gray D.Haddock E Huggard E J.R.Jones E.Montgomery I.Musgrave E Oliveira D.R.Rusby C.Spindloe B.Summers E.Zemaityte Z.Zhang Y.Li P.McKenna D.Neely | 2018 | High Power Laser Science and Engineering2018，6，2： | 3 |
| 2 | In vivo analysis of oligodendrocyte lineage development in postnatal FGF2 null mice显示文摘 | Joshua C.Murtie Yong‐XingZhou Tuan Q.Le Regina C.Armstrong | 2005 | Glia2005，，4： | 1 |
| 3 | Metaxin deficiency alters mitochondrial membrane permeability and leads to resistance to TNF-induced cell killing显示文摘Metaxin,a mitochondrial outer membrane protein,is critical for TNF-induced cell death in L929 cells.Its deficiency,caused by retroviral insertion-mediated mutagenesis,renders L929 cells resistance to TNF killing.In this study,we further characterized metaxin deficiency-caused TNF resistance in parallel with Bcl-X_(L) overexpressionmediated death resistance.We did not find obvious change in mitochondria membrane potential in metaxindeficient(Met^(mut))and Bcl-X_(L)-overexpressing cells,but we did find an increase in the release rate of the mitochondrial membrane potential probe rhodamine 123(Rh123)that was preloaded into mitochondria.In addition,overexpression of a function-interfering mutant of metaxin(MetaΔTM/C)or Bcl-X_(L) in MCF-7.3.28 cells also resulted in an acquired resistance to TNF killing and a faster rate of Rh123 release,indicating a close correlation between TNF resistance and higher rates of the dye release from the mitochondria.The release of Rh123 can be controlled by the mitochondrial membrane permeability transition(PT)pore,as targeting an inner membrane component of the PT pore by cyclosporin A(CsA)inhibited Rh123 release.However,metaxin deficiency and Bcl-X_(L) overexpression apparently affect Rh123 release from a site(s)different from that of CsA,as CsA can overcome their effect.Though both metaxin and Bcl-X_(L) appear to function on the outer mitochondrial membrane,they do not interact with each other.They may use different mechanisms to increase the permeability of Rh123,since previous studies have suggested that metaxin may influence certain outer membrane porins while Bcl-X_(L) may form pores on the outer membrane.The alteration of the mitochondrial outer membrane properties by metaxin deficiency and Bcl-X_(L) overespression,as indicated by a quicker Rh123 release,may be helpful in maintaining mitochondrial integrity. | Koh Ono Xiaofei Wang Sung Ouk Kim Lucas C.Armstrong Paul Bornstein Jiahuai Han | 2010 | Protein & Cell2010，1，2： | 1 |
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