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Desorption dynamics of deuterium in CuCrZr alloy
Thi Nguyen, Lan Anh,Lee, Sanghwa,Noh, S.J.,Lee, S.K.,Park, M.C.,Shu, Wataru,Pitcher, Spencer,Torcy, David,Guillermain, David,Kim, Jaeyong Elsevier 2017 JOURNAL OF NUCLEAR MATERIALS Vol.496 No.-
<P><B>Abstract</B></P> <P>Desorption behavior of deuterium (D<SUB>2</SUB>) in CuCrZr alloy was investigated considering sample thickness, loading and baking temperature of deuterium followed by the ITER scopes. Cylindrical specimens of 1, 3, 5 mm thick with 4 mm diameter were exposed to deuterium at a pressure of 25 bar at 120, 240 and 350 °C for 24 h, then baked at 800 °C in a vacuum chamber maintained at a pressure lower than 10<SUP>−7</SUP> Torr. Deuterium desorption characteristics such as desorption rate and amount of deuterium in the sample were estimated by analyzing the desorption peaks monitored with a residual gas analyzer (RGA), and the trapping energy of deuterium was calculated using thermal desorption spectroscopy (TDS). Secondary ion mass spectroscopy (SIMS) results showed that deuterium atoms embedded in the sample at a depth of less than 15 μm and desorbed as low as 400 °C. All absorbed deuterium atoms in the specimen were completely retrieved by dynamic pumping at 800 °C in 15 min. The desorption rate of deuterium per unit area was inversely proportional to the increment of the thickness of the sample, and was proportional to the loading temperature. Based on the assumption that a uniform distribution of interstitial sites for deuterium follows the Femi-Dirac statistics, the result of TDS demonstrated that the CuCrZr alloy has two types of trapping energies, which were estimated to be 62 and 79 kJ/mol.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Desorption behavior of deuterium in CuCrZr alloys was investigated following the ITER scopes. </LI> <LI> Deuterium was embedded in CuCrZr alloys at a depth of less than 15 μm, and can be completely retrieved in 15 min through dynamic pumping at 800 °C. </LI> <LI> Desorption rate of deuterium was inversely proportional to the increment of the thickness of the sample but proportional to the loading temperature. </LI> <LI> The trapping energies of deuterium in CuCrZr alloys were 62 and 79 kJ/mol. </LI> </UL> </P>
Redditt, Thomas J.,Chung, Eui-Hwan,Karimi, Hana Zand,Rodibaugh, Natalie,Zhang, Yixiang,Trinidad, Jonathan C.,Kim, Jin Hee,Zhou, Qian,Shen, Mingzhe,Dangl, Jeffery L.,Mackey, David,Innes, Roger W. American Society of Plant Biologists 2019 The Plant cell Vol.31 No.11
<P>The <I>Pseudomonas syringae</I> effector protein AvrRpm1 ADP ribosylates RIN4 proteins from Arabidopsis and soybean, which promotes association of RIN4 with EXO70E2 and suppression of callose deposition.</P><P>The <I>Pseudomonas syringae</I> effector protein AvrRpm1 activates the Arabidopsis (<I>Arabidopsis thaliana</I>) intracellular innate immune receptor protein RESISTANCE TO PSEUDOMONAS MACULICOLA1 (RPM1) via modification of a second Arabidopsis protein, RPM1-INTERACTING PROTEIN4 (<I>At</I>RIN4). Prior work has shown that AvrRpm1 induces phosphorylation of <I>At</I>RIN4, but homology modeling indicated that AvrRpm1 may be an ADP-ribosyl transferase. Here, we show that AvrRpm1 induces ADP-ribosylation of RIN4 proteins from both Arabidopsis and soybean (<I>Glycine max</I>) within two highly conserved nitrate-induced (NOI) domains. It also ADP ribosylates at least 10 additional Arabidopsis NOI domain-containing proteins. The ADP-ribosylation activity of AvrRpm1 is required for subsequent phosphorylation on Thr-166 of <I>At</I>RIN4, an event that is necessary and sufficient for RPM1 activation. We also show that the C-terminal NOI domain of AtRIN4 interacts with the exocyst subunits EXO70B1, EXO70E1, EXO70E2, and EXO70F1. Mutation of either EXO70B1 or EXO70E2 inhibited secretion of callose induced by the bacterial flagellin-derived peptide flg22. Substitution of RIN4 Thr-166 with Asp enhanced the association of <I>At</I>RIN4 with EXO70E2, which we posit inhibits its callose deposition function. Collectively, these data indicate that AvrRpm1 ADP-ribosyl transferase activity contributes to virulence by promoting phosphorylation of RIN4 Thr-166, which inhibits the secretion of defense compounds by promoting the inhibitory association of RIN4 with EXO70 proteins.</P><P>[Figure]</P>
Acton, Orb,Dubey, Manish,Weidner, Tobias,O’Malley, Kevin M.,Kim, Tae‐,Wook,Ting, Guy G.,Hutchins, Daniel,Baio, J. E.,Lovejoy, Tracy C.,Gage, Alexander H.,Castner, David G.,Ma, Hong,Jen, Alex K.& WILEY‐VCH Verlag 2011 Advanced functional materials Vol.21 No.8
<P><B>Abstract</B></P><P>An efficient process is developed by spin‐coating a single‐component, self‐assembled monolayer (SAM) to simultaneously modify the bottom‐contact electrode and dielectric surfaces of organic thin‐film transistors (OTFTs). This effi cient interface modifi cation is achieved using <I>n</I>‐alkyl phosphonic acid based SAMs to prime silver bottom‐contacts and hafnium oxide (HfO<SUB>2</SUB>) dielectrics in low‐voltage OTFTs. Surface characterization using near edge X‐ray absorption fi ne structure (NEXAFS) spectroscopy, X‐ray photoelectron spectroscopy (XPS), attenuated total reflectance Fourier transform infrared (ATR‐FTIR) spectroscopy, atomic force microscopy (AFM), and spectroscopic ellipsometry suggest this process yields structurally well‐defi ned phosphonate SAMs on both metal and oxide surfaces. Rational selection of the alkyl length of the SAM leads to greatly enhanced performance for both <I>n</I>‐channel (C<SUB>60</SUB>) and p‐channel (pentacene) based OTFTs. Specifi cally, SAMs of <I>n</I>‐octylphos‐phonic acid (OPA) provide both low‐contact resistance at the bottom‐contact electrodes and excellent interfacial properties for compact semiconductor grain growth with high carrier mobilities. OTFTs based on OPA modifi ed silver electrode/HfO<SUB>2</SUB> dielectric bottom‐contact structures can be operated using < 3V with low contact resistance (down to 700 Ohm‐cm), low subthreshold swing (as low as 75 mV dec<SUP>−1</SUP>), high on/off current ratios of 107, and charge carrier mobilities as high as 4.6 and 0.8 cm<SUP>2</SUP> V<SUP>−1</SUP> s<SUP>−1</SUP>, for C60 and pentacene, respectively. These results demonstrate that this is a simple and efficient process for improving the performance of bottom‐contact OTFTs.</P>
Inhibition of a NEDD8 Cascade Restores Restriction of HIV by APOBEC3G
( David J Stanley ),( Koen Bartholomeeusen ),( David C Crosby ),( Dong Yong Kim ),( Eunju Kwon ),( Linda Yen ),( Nathalie Caretta Cartazo ),( Ming Li ),( Stefanie J?ger ),( Jeremy Mason Herr ),( Fumia 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
Cellular restriction factors help to defend humans against human immunodeficiency virus (HIV). HIV accessory proteins hijack at least three different Cullin-RING ubiquitin ligases, which must be activated by the small ubiquitin-like protein NEDD8, in order to counteract host cellularrestriction factors. We found that conjugation of NEDD8 to Cullin-5 by the NEDD8-conjugating enzyme UBE2F is required for HIV Vif-mediated degradation of the host restriction factor APOBEC3G (A3G). Pharmacological inhibition of the NEDD8 E1 by MLN4924 or knockdown of either UBE2F or its RING-protein binding partner RBX2 bypasses the effect of Vif, restoring the restriction of HIV by A3G. NMR mapping and mutational analyses define specificity determinants of the UBE2F NEDD8 cascade. These studies demonstrate that disrupting host NEDD8 cascades presents a novel antiretroviral therapeutic approach enhancing the ability of the immune system to combat HIV.
Degradation of thin carbon-backed lithium fluoride targets bombarded by 68 MeV 17O beams
김용현,Davids B.,Williams M.,Hudson K.H.,Upadhyayula S.,Alcorta M.,Machule P.,Esker N.E.,Griffin C.J.,Williams J.,Yates D.,Lennarz A.,Angus C.,Hackman G.,김동건,J. Son,Park J.,Pak K.,김용균 한국원자력학회 2023 Nuclear Engineering and Technology Vol.55 No.3
To analyze the cause of the destruction of thin, carbon-backed lithium fluoride targets during a measurement of the fusion of 7Li and 17O, we estimate theoretically the lifetimes of carbon and LiF films due to sputtering, thermal evaporation, and lattice damage and compare them with the lifetime observed in the experiment. Sputtering yields and thermal evaporation rates in carbon and LiF films are too low to play significant roles in the destruction of the targets.We estimate the lifetime of the target due to lattice damage of the carbon backing and the LiF film using a previously reported model. In the experiment, elastically scattered target and beam ions were detected by surface silicon barrier (SSB) detectors so that the product of the beam flux and the target density could be monitored during the experiment. The areas of the targets exposed to different beam intensities and fluences were degraded and then perforated, forming holes with a diameter around the beam spot size. Overall, the target thickness tends to decrease linearly as a function of the beam fluence. However, the thickness also exhibits an increasing interval after SSB counts per beam ion decreases linearly, extending the target lifetime. The lifetime of thin LiF film as determined by lattice damage is calculated for the first time using a lattice damage model, and the calculated lifetime agrees well with the observed target lifetime during the experiment. In experiments using a thin LiF target to induce nuclear reactions, this study suggests methods to predict the lifetime of the LiF film and arrange the experimental plan for maximum efficiency
s -wave scattering lengths for the Be7+p system from an R -matrix analysis
Paneru, S. N.,Brune, C. R.,Giri, R.,Livesay, R. J.,Greife, U.,Blackmon, J. C.,Bardayan, D. W.,Chipps, K. A.,Davids, B.,Connolly, D. S.,Chae, K. Y.,Champagne, A. E.,Deibel, C.,Jones, K. L.,Johnson, M. American Physical Society 2019 Physical Review C Vol.99 No.4
VEGF-Induced Vascular Permeability Is Mediated by FAK
Chen, X.,Nam, J.O.,Jean, C.,Lawson, C.,Walsh, Colin T.,Goka, E.,Lim, S.T.,Tomar, A.,Tancioni, I.,Uryu, S.,Guan, J.L.,Acevedo, Lisette M.,Weis, Sara M.,Cheresh, David A.,Schlaepfer, David D. Cell Press 2012 DEVELOPMENTAL CELL Vol.22 No.1
Endothelial cells (ECs) form cell-cell adhesive junctional structures maintaining vascular integrity. This barrier is dynamically regulated by vascular endothelial growth factor (VEGF) receptor signaling. We created an inducible knockin mouse model to study the contribution of the integrin-associated focal adhesion tyrosine kinase (FAK) signaling on vascular function. Here we show that genetic or pharmacological FAK inhibition in ECs prevents VEGF-stimulated permeability downstream of VEGF receptor or Src tyrosine kinase activation in vivo. VEGF promotes tension-independent FAK activation, rapid FAK localization to cell-cell junctions, binding of the FAK FERM domain to the vascular endothelial cadherin (VE-cadherin) cytoplasmic tail, and direct FAK phosphorylation of β-catenin at tyrosine-142 (Y142) facilitating VE-cadherin-β-catenin dissociation and EC junctional breakdown. Kinase inhibited FAK is in a closed conformation that prevents VE-cadherin association and limits VEGF-stimulated β-catenin Y142 phosphorylation. Our studies establish a role for FAK as an essential signaling switch within ECs regulating adherens junction dynamics.