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On the dust abundance gradients in late-type galaxies: I. Effects of destruction and growth of dust in the interstellar medium  [PDF]
Lars Mattsson,Anja C. Andersen,Joakim D. Munkhammar
Physics , 2012, DOI: 10.1111/j.1365-2966.2012.20575.x
Abstract: We present basic theoretical constraints on the effects of destruction by supernovae (SNe) and growth of dust grains in the interstellar medium (ISM) on the radial distribution of dust in late-type galaxies. The radial gradient of the dust-to-metals ratio is shown to be essentially flat (zero) if interstellar dust is not destroyed by SN shock waves and all dust is produced in stars. If there is net dust destruction by SN shock waves, the dust-to-metals gradient is flatter than or equal to the metallicity gradient (assuming the gradients have the same sign). Similarly, if there is net dust growth in the ISM, then the dust-to-metals gradient is steeper than or equal to the metallicity gradient. The latter result implies that if dust gradients are steeper than metallicity gradients, i.e., the dust-to-metals gradients are not flat, then it is unlikely dust destruction by SN shock waves is an efficient process, while dust growth must be a significant mechanism for dust production. Moreover, we conclude that dust-to-metals gradients can be used as a diagnostic for interstellar dust growth in galaxy discs, where a negative slope indicates dust growth.
Formation of late-type spiral galaxies: gas return from stellar populations regulates disk destruction and bulge growth  [PDF]
Marie Martig,Frederic Bournaud
Physics , 2009, DOI: 10.1088/2041-8205/714/2/L275
Abstract: Spiral galaxies have most of their stellar mass in a large rotating disk, and only a modest fraction in a central spheroidal bulge. This poses a major challenge for cosmological models of galaxy formation. Galaxies form at the centre of dark matter halos through a combination of hierarchical merging and gas accretion along cold streams, and should rapidly grow their bulge through mergers and instabilities. Cosmological simulations predict galaxies to have most of their mass in the central bulge, and therefore an angular momentum much below the observed level, except in dwarf galaxies. We propose that the continuous return of fresh gas by stellar populations over cosmic times could solve this issue. A population of stars formed at a given instant typically returns half of its initial mass in the form of gas over 10 billion years, and the process is not dominated by rapid supernovae explosions but by the long-term mass-loss from low- and intermediate-mass stars. Using simulations of galaxy formation, we show that this recycling of gas can strongly affect the structural evolution of massive galaxies, potentially solving the bulge fraction issue: we find that the bulge-to-disk ratio of a massive galaxy can be divided by a factor of 3. The continuous recycling of baryons through star formation and stellar mass loss helps the growth of disks and their survival to interactions and mergers. Instead of forming only early-type, spheroid-dominated galaxies (S0 and ellipticals), the standard cosmological model can then successfully account for massive late-type, disk-dominated spiral galaxies (Sb-Sc).
APCcdh1 Mediates Degradation of the Oncogenic Rho-GEF Ect2 after Mitosis  [PDF]
Caroline Liot, Laetitia Seguin, Aurélie Siret, Catherine Crouin, Susanne Schmidt, Jacques Bertoglio
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023676
Abstract: Background Besides regulation of actin cytoskeleton-dependent functions, Rho GTPase pathways are essential to cell cycle progression and cell division. Rho, Rac and Cdc42 regulate G1 to S phase progression and are involved in cytokinesis. RhoA GDP/GTP cycling is required for normal cytokinesis and recent reports have shown that the exchange factor Ect2 and the GTPase activating protein MgcRacGAP regulate RhoA activity during mitosis. We previously showed that the transcription factors E2F1 and CUX1 regulate expression of MgcRacGAP and Ect2 as cells enter S-phase. Methodology/Principal Findings We now report that Ect2 is subject to proteasomal degradation after mitosis, following ubiquitination by the APC/C complex and its co-activator Cdh1. A proper nuclear localization of Ect2 is necessary for its degradation. APC-Cdh1 assembles K11-linked poly-ubiquitin chains on Ect2, depending upon a stretch of ~25 amino acid residues that contain a bi-partite NLS, a conventional D-box and two TEK-like boxes. Site-directed mutagenesis of target sequences generated stabilized Ect2 proteins. Furthermore, such degradation-resistant mutants of Ect2 were found to activate RhoA and subsequent signalling pathways and are able to transform NIH3T3 cells. Conclusions/Significance Our results identify Ect2 as a bona fide cell cycle-regulated protein and suggest that its ubiquitination-dependent degradation may play an important role in RhoA regulation at the time of mitosis. Our findings raise the possibility that the overexpression of Ect2 that has been reported in some human tumors might result not only from deregulated transcription, but also from impaired degradation.
Microarray Analysis of Tomato’s Early and Late Wound Response Reveals New Regulatory Targets for Leucine Aminopeptidase A  [PDF]
Melissa A. Scranton, Jonathan H. Fowler, Thomas Girke, Linda L. Walling
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0077889
Abstract: Wounding due to mechanical injury or insect feeding causes a wide array of damage to plant cells including cell disruption, desiccation, metabolite oxidation, and disruption of primary metabolism. In response, plants regulate a variety of genes and metabolic pathways to cope with injury. Tomato (Solanum lycopersicum) is a model for wound signaling but few studies have examined the comprehensive gene expression profiles in response to injury. A cross-species microarray approach using the TIGR potato 10-K cDNA array was analyzed for large-scale temporal (early and late) and spatial (locally and systemically) responses to mechanical wounding in tomato leaves. These analyses demonstrated that tomato regulates many primary and secondary metabolic pathways and this regulation is dependent on both timing and location. To determine if LAP-A, a known modulator of wound signaling, influences gene expression beyond the core of late wound-response genes, changes in RNAs from healthy and wounded Leucine aminopeptidase A-silenced (LapA-SI) and wild-type (WT) leaves were examined. While most of the changes in gene expression after wounding in LapA-SI leaves were similar to WT, overall responses were delayed in the LapA-SI leaves. Moreover, two pathogenesis-related 1 (PR-1c and PR-1a2) and two dehydrin (TAS14 and Dhn3) genes were negatively regulated by LAP-A. Collectively, this study has shown that tomato wound responses are complex and that LAP-A’s role in modulation of wound responses extends beyond the well described late-wound gene core.
High Resolution Spectroscopy and Spectropolarimetry of some late F-/early G-type sun-like stars as targets for Zeeman Doppler imaging  [PDF]
Ian Waite,Stephen Marsden,Brad Carter,Evelyne Alecian,Carolyn Brown,Donna Burton,Rhodes Hart
Physics , 2011, DOI: 10.1071/AS11025
Abstract: High resolution spectroscopy and spectropolarimetry have been undertaken at the Anglo-Australian Telescope in order to identify suitable targets for magnetic studies of young sun-like stars, for the proxy study of early solar evolution. This study involved the investigation of some variable late F-/early G-type sun-like stars originally identified by the Hipparcos mission. Of the 38 stars observed for this study, HIP 31021, HIP 64732, HIP 73780 were found to be spectroscopic binary stars while HIP 19072, HIP 67651 and HIP 75636 are also likely to be binaries while HIP 33111 could even be a triple system. Magnetic fields were detected on a number of the survey stars: HIP 21632, HIP 43720, HIP 48770, HIP 62517, HIP 71933, HIP 77144, HIP 89829, HIP 90899 and HIP 105388, making these stars good candidates for follow-up Zeeman Doppler imaging studies.
On the timing and duration of the destruction of the North China Craton
YiGang Xu,HongYan Li,ChongJin Pang,Bin He
Chinese Science Bulletin , 2009, DOI: 10.1007/s11434-009-0346-5
Abstract: The timing and duration of the destruction of the North China Craton, which is pivotal to understanding the destruction mechanism and its geodynamic controlling factors, still remain controversial. On the basis of the principles of magma genesis and evolution, first we outline magmatic expressions that can be related to cratonic destruction, then use magmatic and basin evolution trends to constrain the timescale of the lithospheric thinning in North China. The main conclusions include: (1) the thinning of the lithosphere beneath the North China Craton might have started, at least locally, since late Carboniferous-late Triassic, attained its climax during the late Jurassic-early Cretaceous, and continued till the end of late Cretaceous-early Cenozoic. The destruction of the North China Craton was a relatively slow, rather than a dramatic process. (2) The weakened lithospheric zones along the margins and interiors of the craton played an important role in cratonic destruction, partly accounting for the heterogeneous pattern of cratonic destruction. (3) The tectonic factors that controlled the destruction of the North China Craton may be multiple. The late Carboniferous southward subduction of the Paleo-Asian plate and the late Triassic collision between North China and South China may have re-activated the craton by influencing the thermal and integral structure of the craton. The Pacific subduction underneath the eastern Asian continent played a determinant role in the cratonic destruction, governing the distribution patterns of post-Mesozoic basins and major tectonic configuration, temporal change of magmatism and formation of the North-South gravity lineament.
DESTRUCTION OF LARGE NETWORKS  [PDF]
P. A. Golovinsky
Scientific Herald of the Voronezh State University of Architecture and Civil Engineering , 2011,
Abstract: Background. Interest in the problem of network reliability increased rapidly owing to the new field of application, including computer and transport networks, as well as social and innovation networks. Models and algorithms of analysis of network destruction dynamics are not sufficiently advanced. In present paper, the simplest — epidemic — type of destruction is considered.Results and conclusions. Epidemic type of network destruction is observed when destruction of the series of network nodes in certain step causes destruction of all the adjacent nodes in the next step of the process. The simple algorithm of calculation of step-by-step destruction of networks in the form of graphs and directed graphs was constructed with the aid of adjacency matrices. General recommendations on efficient network protection by transition from the initial graph to the frame are given on the basis of the analysis of matrix solution and graph structure. It is established that efficiency of operation and reliability of the network are interdependent and cannot be provided simultaneously. The relation between large network reliability and problem of globalization is remarked.
Nonlinear coherent destruction of tunneling  [PDF]
Xiaobing Luo,Qiongtao Xie,Biao Wu
Physics , 2007, DOI: 10.1103/PhysRevA.76.051802
Abstract: We study theoretically two coupled periodically-curved optical waveguides with Kerr nonlinearity. We find that the tunneling between the waveguides can be suppressed in a wide range of parameters due to nonlinearity. Such suppression of tunneling is different from the coherent destruction of tunneling in a linear medium, which occurs only at the isolated degeneracy point of the quasienergies. We call this novel suppression nonlinear coherent destruction of tunneling.
Destruction of states in quantum mechanics  [PDF]
P. Caban,J. Rembielinski,K. A. Smolinski,Z. Walczak
Mathematics , 2001, DOI: 10.1088/0305-4470/35/14/308
Abstract: A description of destruction of states on the grounds of quantum mechanics rather than quantum field theory is proposed. Several kinds of maps called supertraces are defined and used to describe the destruction procedure. The introduced algorithm can be treated as a supplement to the von Neumann-Lueders measurement. The discussed formalism may be helpful in a description of EPR type experiments and in quantum information theory.
The function of APC/CCdh1 in cell cycle and beyond
Min Li, Pumin Zhang
Cell Division , 2009, DOI: 10.1186/1747-1028-4-2
Abstract: Two ubiquitin E3-ligase complexes, SCF (Skp1/CUL1/F-box protein) and APC/C (anaphase promoting complex/cyclosome), control the timely transitions of cell cycle phases by promoting the degradation of many key cell cycle regulators. SCF complex mainly functions in G1, S and early M phases, whereas APC/C regulates mitosis including metaphase-anaphase transition and mitotic exit and maintains G1 phase [1,2]. APC/C is a large (1.5 MDa complex) composed of at lease 11 core subunits. It relies on two WD-40 repeat-containing adaptor proteins, Cdc20/fizzy(fzy)/p55CDC and Hct1/srw1/fizzy-related(fzr)/Cdh1, to engage with its substrates. Destruction box (RXXLXXXXN/D/E) and KEN box are motifs frequently found in APC's substrates, but other motifs are also possible for recognition by APCCdc20 or APCCdh1 [3]. The consensus sequence of destruction box can be found in many proteins. However, not all of these proteins are APC's substrates. Thus, there must be other sequence constrains we do not understand yet that define true APC substrates. Moreover, some substrates only have an RxxL motif and yet are recognized by APC, indicating the last amino acid in the consensus is not stringently conserved.APCCdc20 initiates the metaphase-anaphase transition through mediating the ubiquitination and degradation of cyclin B1 and securin. To prevent premature separation of sister chromatids and mitotic exit, APCCdc20 is inhibited by Mad2 and BubR1 through the spindle assembly checkpoint mechanism [4-9]. Only when the sister chromatids are aligned at the metaphase plate and have established bivalent spindle attachment can the inhibition of APC/Cdc20 be released. In contrast to APCCdc20, APCCdh1 is inactive in early mitosis [3] when it is inhibited by phosphorylation [10] and binding of Nup90/Rae1 complex [11,12]. APCCdh1 only becomes active from late mitosis to G1. The difference in the timing of activation between APCCdc20 and APCCdh1 suggests a functional division between the two E3 ubiquitin l
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