11,155 research outputs found

    Fluctuation-induced tunneling conduction through RuO2_2 nanowire contacts

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    A good understanding of the electronic conduction processes through nanocontacts is a crucial step for the implementation of functional nanoelectronic devices. We have studied the current-voltage (II-VV) characteristics of nanocontacts between single metallic RuO2_2 nanowires (NWs) and contacting Au electrodes which were pre-patterned by simple photolithography. Both the temperature behavior of contact resistance in the low-bias voltage ohmic regime and the II-VV curves in the high-bias voltage non-ohmic regime have been investigated. We found that the electronic conduction processes in the wide temperature interval 1--300 K can be well described by the fluctuation-induced tunneling (FIT) conduction theory. Taken together with our previous work (Lin {\it et al.}, Nanotechnology {\bf 19}, 365201 (2008)) where the nanocontacts were fabricated by delicate electron-beam lithography, our study demonstrates the general validity of the FIT model in characterizing electronic nanocontacts.Comment: 6 pages, 5 figure

    Reversibility and Improved Hydrogen Release of Magnesium Borohydride

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    Desorption and subsequent rehydrogenation of Mg(BH_4)_2 with and without 5 mol % TiF_3 and ScCl_3 have been investigated. Temperature programmed desorption (TPD) experiments revealed a significant increase in the rate of desorption as well as the weight percentage of hydrogen released with additives upon heating to 300 °C. Stable Mg(B_xH_y)_n intermediates were formed at 300 °C, whereas MgB_2 was the major product when heated to 600 °C. These samples were then rehydrogenated and subsequently characterized with powder X-ray diffraction (pXRD), Raman, and NMR spectroscopy. We confirmed significant conversion of MgB_2 to fully hydrogenated Mg(BH_4)_2 for the sample with and without additives. TPD and NMR studies revealed that the additives have a significant effect on the reaction pathway during both dehydrogenation and rehydrogenation reactions. This work suggests that the use of additives may provide a valid pathway for improving intrinsic hydrogen storage properties of magnesium borohydride

    Inhibition of Acetylcholinesterase by N-Alkylpyridinium and N-Alkylpyridinium-2-aldoxime Salts

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    The interaction of a series of N-a1kylpyridinium and N-alkylpyridinium- 2-aldoxime salts with bovine erythrocyte acetylcholinesterase was investigated for inhibition of the hydrolysis of the substrates acetylcholine and dimethylaminoethyl acetate. The compounds cause a mixed inhibition of the acetylcholine hydrolysis which is interpreted as an interaction with the free enzyme (competitive component) and with the acetylenzyme (non- competitive component). The results suggest that the compounds have a higher affinity for the free enzyme than for the acetyl- enzyme. Enlargement of the alkyl-group increases the binding capacity to the free enzyme. The aldoxime group hardly effects the binding to the free enzyme, but tends to increase the binding to the acetyl-enzyme. Some results obtained with dimethylaminoethyl acetate support the mechanism of inhibition as proposed from acetylcholine hydrolysis inhibition. In contrast to this mechanism some compounds do not influence or even increase the maximum velocity of the dimethylaminoethyl acetate hydrolysis. It is suggested that a ternary complex of enzyme, substrate and pyridinium compound may be formed from which, in case of dimethylaminoethyl acetate, the enzyme is more rapidly acetylated

    Inhibition of Acetylcholinesterase by N-Alkylpyridinium and N-Alkylpyridinium-2-aldoxime Salts

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    The interaction of a series of N-a1kylpyridinium and N-alkylpyridinium- 2-aldoxime salts with bovine erythrocyte acetylcholinesterase was investigated for inhibition of the hydrolysis of the substrates acetylcholine and dimethylaminoethyl acetate. The compounds cause a mixed inhibition of the acetylcholine hydrolysis which is interpreted as an interaction with the free enzyme (competitive component) and with the acetylenzyme (non- competitive component). The results suggest that the compounds have a higher affinity for the free enzyme than for the acetyl- enzyme. Enlargement of the alkyl-group increases the binding capacity to the free enzyme. The aldoxime group hardly effects the binding to the free enzyme, but tends to increase the binding to the acetyl-enzyme. Some results obtained with dimethylaminoethyl acetate support the mechanism of inhibition as proposed from acetylcholine hydrolysis inhibition. In contrast to this mechanism some compounds do not influence or even increase the maximum velocity of the dimethylaminoethyl acetate hydrolysis. It is suggested that a ternary complex of enzyme, substrate and pyridinium compound may be formed from which, in case of dimethylaminoethyl acetate, the enzyme is more rapidly acetylated

    Ubiquitin-based probes prepared by total synthesis to profile the activity of deubiquitinating enzymes

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    Epitope-tagged active-site-directed probes are widely used to visualize the activity of deubiquitinases (DUBs) in cell extracts, to investigate the specificity and potency of small-molecule DUB inhibitors, and to isolate and identify DUBs by mass spectrometry. With DUBs arising as novel potential drug targets, probes are required that can be produced in sufficient amounts and to meet the specific needs of a given experiment. The established method for the generation of DUB probes makes use of labor-intensive intein-based methods that have inherent limitations concerning the incorporation of unnatural amino acids and the amount of material that can be obtained. Here, we describe the total chemical synthesis of active-site-directed probes and their application to activity-based profiling and identification of functional DUBs. This synthetic methodology allowed the easy incorporation of desired tags for specific applications, for example, fluorescent reporters, handles for immunoprecipitation or affinity pull-down, and cleavable linkers. Additionally, the synthetic method can be scaled up to provide significant amounts of probe. Fluorescent ubiquitin probes allowed faster, in-gel detection of active DUBs, as compared to (immuno)blotting procedures. A biotinylated probe holding a photocleavable linker enabled the affinity pull-down and subsequent mild, photorelease of DUBs. Also, DUB activity levels were monitored in response to overexpression or knockdown, and to inhibition by small molecules. Furthermore, fluorescent probes revealed differential DUB activity profiles in a panel of lung and prostate cancer cells

    Sharing digital object across data infrastructures using Named Data Networking (NDN)

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    Data infrastructures manage the life cycle of digital assets and allow users to efficiently discover them. To improve the Findability, Accessibility, Interoperability and Re-usability (FAIRness) of digital assets, a data infrastructure needs to provide digital assets with not only rich meta information and semantics contexts information but also globally resolvable identifiers. The Persistent Identifiers (PIDs), like Digital Object Identifier (DOI) are often used by data publishers and infrastructures. The traditional IP network and client-server model can potentially cause congestion and delays when many consumers simultaneously access data. In contrast, Information-Centric Networking (ICN) technologies such as Named Data Networking (NDN) adopt a data-centric approach where digital data objects, once requested, may be stored on intermediate hops in the network. Consecutive requests for that unique digital object are then made available by these intermediate hops (caching). This approach distributes traffic load more efficient and reliable compared to host-to-host connection-oriented techniques and demonstrates attractive opportunities for sharing digital objects across distributed networks. However, such an approach also faces several challenges. It requires not only an effective translation between the different naming schemas among PIDs and NDN, in particular for supporting PIDs from different publishers or repositories. Moreover, the planning and configuration of an ICN environment for distributed infrastructures are lacking an automated solution. To bridge the gap, we propose an ICN planning service with specific consideration of interoperability across PID schemas in the Cloud environment

    The spliceosome-activating complex: molecular mechanisms underlying the function of a pleiotropic regulator

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    Correct interpretation of the coding capacity of RNA polymerase II transcribed eukaryotic genes is determined by the recognition and removal of intronic sequences of pre-mRNAs by the spliceosome. Our current knowledge on dynamic assembly and subunit interactions of the spliceosome mostly derived from the characterization of yeast, Drosophila, and human spliceosomal complexes formed on model pre-mRNA templates in cell extracts. In addition to sequential structural rearrangements catalyzed by ATP-dependent DExH/D-box RNA helicases, catalytic activation of the spliceosome is critically dependent on its association with the NineTeen Complex (NTC) named after its core E3 ubiquitin ligase subunit PRP19. NTC, isolated recently from Arabidopsis, occurs in a complex with the essential RNA helicase and GTPase subunits of the U5 small nuclear RNA particle that are required for both transesterification reactions of splicing. A compilation of mass spectrometry data available on the composition of NTC and spliceosome complexes purified from different organisms indicates that about half of their conserved homologs are encoded by duplicated genes in Arabidopsis. Thus, while mutations of single genes encoding essential spliceosome and NTC components lead to cell death in other organisms, differential regulation of some of their functionally redundant Arabidopsis homologs permits the isolation of partial loss of function mutations. Non-lethal pleiotropic defects of these mutations provide a unique means for studying the roles of NTC in co-transcriptional assembly of the spliceosome and its crosstalk with DNA repair and cell death signaling pathways
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