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  • 1
    Publication Date: 2012-03-14
    Description: Saccharomyces cerevisiae Mph1 is a 3–5' DNA helicase, required for the maintenance of genome integrity. In order to understand the ATPase/helicase role of Mph1 in genome stability, we characterized its helicase activity with a variety of DNA substrates, focusing on its action on junction structures containing three or four DNA strands. Consistent with its 3' to 5' directionality, Mph1 displaced 3'-flap substrates in double-fixed or equilibrating flap substrates. Surprisingly, Mph1 displaced the 5'-flap strand more efficiently than the 3' flap strand from double-flap substrates, which is not expected for a 3–5' DNA helicase. For this to occur, Mph1 required a threshold size (〉5 nt) of 5' single-stranded DNA flap. Based on the unique substrate requirements of Mph1 defined in this study, we propose that the helicase/ATPase activity of Mph1 play roles in converting multiple-stranded DNA structures into structures cleavable by processing enzymes such as Fen1. We also found that the helicase activity of Mph1 was used to cause structural alterations required for restoration of replication forks stalled due to damaged template. The helicase properties of Mph1 reported here could explain how it resolves D-loop structure, and are in keeping with a model proposed for the error-free damage avoidance pathway.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
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  • 2
    Publication Date: 2014-08-28
    Description: Despite the noble electronic properties of graphene, its industrial application has been hindered mainly by the absence of a stable means of producing a band gap at the Dirac point (DP). We report a new route to open a band gap (E g ) at DP in a controlled way by depositing positively charged Na + ions on single layer graphene formed on 6H-SiC(0001) surface. The doping of low energy Na + ions is found to deplete the π * band of graphene above the DP, and simultaneously shift the DP downward away from Fermi energy indicating the opening of E g . The band gap increases with increasing Na + coverage with a maximum E g ≥ 0.70   eV . Our core-level data, C 1 s , Na 2 p , and Si 2 p , consistently suggest that Na + ions do not intercalate through graphene, but produce a significant charge asymmetry among the carbon atoms of graphene to cause the opening of a band gap. We thus provide a reliable way of producing and tuning the band gap of graphene by using Na + ions, which may play a vital role in utilizing graphene in future nano-electronic devices.
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-13
    Description: Ice accretion has a negative impact on critical infrastructure, as well as a range of commercial and residential activities. Icephobic surfaces are defined by an ice adhesion strength ice 〈 100 kPa. However, the passive removal of ice requires much lower values of ice , such as on airplane wings or power lines ( ice 〈 20 kPa). Such low ice values are scarcely reported, and robust coatings that maintain these low values have not been reported previously. We show that, irrespective of material chemistry, by tailoring the cross-link density of different elastomeric coatings and by enabling interfacial slippage, it is possible to systematically design coatings with extremely low ice adhesion ( ice 〈 0.2 kPa). These newfound mechanisms allow for the rational design of icephobic coatings with virtually any desired ice adhesion strength. By using these mechanisms, we fabricate extremely durable coatings that maintain ice 〈 10 kPa after severe mechanical abrasion, acid/base exposure, 100 icing/deicing cycles, thermal cycling, accelerated corrosion, and exposure to Michigan wintery conditions over several months.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 4
    Publication Date: 2011-08-06
    Description: Formation of myelin, the electrical insulation on axons produced by oligodendrocytes, is controlled by complex cell-cell signaling that regulates oligodendrocyte development and myelin formation on appropriate axons. If electrical activity could stimulate myelin induction, then neurodevelopment and the speed of information transmission through circuits could be modified by neural activity. We find that release of glutamate from synaptic vesicles along axons of mouse dorsal root ganglion neurons in culture promotes myelin induction by stimulating formation of cholesterol-rich signaling domains between oligodendrocytes and axons, and increasing local synthesis of the major protein in the myelin sheath, myelin basic protein, through Fyn kinase-dependent signaling. This axon-oligodendrocyte signaling would promote myelination of electrically active axons to regulate neural development and function according to environmental experience.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482340/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482340/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wake, Hiroaki -- Lee, Philip R -- Fields, R Douglas -- Z99 HD999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1647-51. doi: 10.1126/science.1206998. Epub 2011 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nervous System Development and Plasticity Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817014" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Axons/*physiology ; Calcium/metabolism ; Calcium Signaling ; Cell Differentiation ; Cells, Cultured ; Electric Stimulation ; Ganglia, Spinal/cytology/embryology ; Glutamic Acid/metabolism ; Mice ; Myelin Basic Protein/*biosynthesis/genetics/metabolism ; Myelin Sheath/*physiology ; Neural Stem Cells/cytology/metabolism ; Oligodendroglia/cytology/*metabolism ; Proto-Oncogene Proteins c-fyn/metabolism ; Receptors, Transferrin/metabolism ; Signal Transduction ; Synaptic Transmission ; Synaptic Vesicles/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-04-04
    Description: Mammalian acyl-CoA thioesterases (Acots) catalyze the hydrolysis of fatty acyl-CoAs to form free fatty acids plus CoA, but their metabolic functions remain undefined. Thioesterase superfamily member 1 (Them1; synonyms Acot11, StarD14, and brown fat inducible thioesterase) is a long-chain fatty acyl-CoA thioesterase that is highly expressed in brown adipose tissue and is regulated by both ambient temperature and food consumption. Here we show that Them1−/− mice were resistant to diet-induced obesity despite greater food consumption. Them1−/− mice exhibited increased O2 consumption and heat production, which were accompanied by increased rates of fatty acid oxidation in brown adipose tissue and up-regulation of genes that promote energy expenditure. Them1−/− mice were also protected against diet-induced inflammation in white adipose tissue, as well as hepatic steatosis, and demonstrated improved glucose homeostasis. The absence of Them1 expression in vivo and in cell culture led to markedly attenuated diet- or chemically induced endoplasmic reticulum stress responses, providing a mechanism by which Them1 deficiency protects against insulin resistance and lipid deposition. Taken together, these data suggest that Them1 functions to decrease energy consumption and conserve calories. In the setting of nutritional excess, the overproduction of free fatty acids by Them1 provokes insulin resistance that is associated with inflammation and endoplasmic reticulum stress.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 6
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    Propellants, Explosives, Pyrotechnics 21 (1996), S. 59-63 
    ISSN: 0721-3115
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: A well-characterized shaped charge was used to study the influence of asymmetrical initiation on the jet. An experimental study yielded flash radiographs of the jets from charges fired with the initiation point offset 2, 4, 6, 8 and 10 mm, respectively, from the central axis. The axial and lateral velocities of the jet particles were determined from the sets of radiographs. In a previous paper it was hypothesized that a simple relationship might exist between the departure vectors of the jet particles and the geometry of the impingement of the detonation front on the liner. Any part of the jet from an asymmetrically initiated shaped charge departs at an angle determined by the difference between the current angle between the actual detonation wave where it contacts the liner, and that which would have arisen had the initiation been perfectly axial. We set up a simple computer code which evaluates, for any given initiation offset distance, the instantaneous angles between the detonation front and the successive elements of the liner which are encountered as the wave sweeps along it. Since it is possible to map particle velocities in the jet on to those regions of the liner where they originated, simulated sets of axial and lateral jet velocities were readily generated. Agreement between theory and experiment is sufficiently close to suggest that our approximation is useful and can assist in understanding the jet dynamics of asymmetrically initiated shaped charges.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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  • 7
    Publication Date: 2019
    Description: Abstract We performed the first systematic analysis of pickup ion (PUI) cutoff speed variations, across compression regions and due to fast fluctuations in solar wind (SW) speed and magnetic field strength. This study is motivated by the need to remove or correct for systematic effects on the determination of the interstellar flow longitude based on the longitudinal variation of the PUI cutoff. Using 2007–2014 STEREO A PLASTIC observations, we identified SW compression regions and accumulated the contained PUI velocity distributions in a superposed epoch analysis. The shift of the cutoff in velocity, interpreted as PUI energization, varies systematically across the compression region and increases approximately linearly with the speed gradient of the compression. Additionally, the shift remains positive into the negative speed gradient at the beginning of the rarefaction region. A similar response is found when PUI distributions are sorted according to the strength of fast fluctuations in SW speed, density, and magnetic field strength. These parameters remain high in the first part of the rarefaction region, suggesting a possible PUI energization through compressive turbulence. Based on these results, we removed the strongest compression regions from the interstellar flow analysis, finding no significant change in direction or uncertainty. Thus, we have revealed the influence of adiabatic compression and compressive turbulence, increasing the PUI cutoff energy, and we have demonstrated that the determination of the interstellar inflow direction via analysis of PUI distributions is robust for a multiyear data set, even in the presence of SW interaction regions.
    Print ISSN: 2169-9380
    Electronic ISSN: 2169-9402
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 8
    Publication Date: 2014-08-25
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
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  • 9
    Publication Date: 2011-06-22
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 2011-07-13
    Description: Homeostatic mechanisms are required to control formation and maintenance of synaptic connections to maintain the general level of neural impulse activity within normal limits. How genes controlling these processes are co-coordinately regulated during homeostatic synaptic plasticity is unknown. MicroRNAs (miRNAs) exert regulatory control over mRNA stability and translation and may contribute to local and activity-dependent posttranscriptional control of synapse-associated mRNAs. However, identifying miRNAs that function through posttranscriptional gene silencing at synapses has remained elusive. Using a bioinformatics screen to identify sequence motifs enriched in the 3′UTR of rapidly destabilized mRNAs, we identified a developmentally and activity-regulated miRNA (miR-485) that controls dendritic spine number and synapse formation in an activity-dependent homeostatic manner. We find that many plasticity-associated genes contain predicted miR-485 binding sites and further identify the presynaptic protein SV2A as a target of miR-485. miR-485 negatively regulated dendritic spine density, postsynaptic density 95 (PSD-95) clustering, and surface expression of GluR2. Furthermore, miR-485 overexpression reduced spontaneous synaptic responses and transmitter release, as measured by miniature excitatory postsynaptic current (EPSC) analysis and FM 1–43 staining. SV2A knockdown mimicked the effects of miR-485, and these effects were reversed by SV2A overexpression. Moreover, 5 d of increased synaptic activity induced homeostatic changes in synaptic specializations that were blocked by a miR-485 inhibitor. Our findings reveal a role for this previously uncharacterized miRNA and the presynaptic protein SV2A in homeostatic plasticity and nervous system development, with possible implications in neurological disorders (e.g., Huntington and Alzheimer's disease), where miR-485 has been found to be dysregulated.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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