3,964 research outputs found

    Radio Band Observations of Blazar Variability

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    The properties of blazar variability in the radio band are studied using the unique combination of temporal resolution from single dish monitoring and spatial resolution from VLBA imaging; such measurements, now available in all four Stokes parameters, together with theoretical simulations, identify the origin of radio band variability and probe the characteristics of the radio jet where the broadband blazar emission originates. Outbursts in total flux density and linear polarization in the optical-to-radio bands are attributed to shocks propagating within the jet spine, in part based on limited modeling invoking transverse shocks; new radiative transfer simulations allowing for shocks at arbitrary angle to the flow direction confirm this picture by reproducing the observed centimeter-band variations observed more generally, and are of current interest since these shocks may play a role in the gamma-ray flaring detected by Fermi. Recent UMRAO multifrequency Stokes V studies of bright blazars identify the spectral variability properties of circular polarization for the first time and demonstrate that polarity flips are relatively common. All-Stokes data are consistent with the production of circular polarization by linear-to-circular mode conversion in a region that is at least partially self-absorbed. Detailed analysis of single-epoch, multifrequency, all-Stokes VLBA observations of 3C 279 support this physical picture and are best explained by emission from an electron-proton plasma.Comment: 6 pages, 5 figures, uses, jaa.sty. Invited talk presented at the conference Multifrequency Variability of Blazars, Guangzhou, China, September 22-24, 2010. To appear in J. Astrophys. Ast

    Nine new species of Begonia (Begoniaceae) from South and West Sulawesi, Indonesia

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    Nine new species of Begonia (Begoniaceae), Begonia comestibilis D.C.Thomas & Ardi, B. insueta D.C.Thomas & Ardi, B. lasioura D.C.Thomas & Ardi, B. nobmanniae D.C.Thomas & Ardi, B. prionota D.C.Thomas & Ardi, B. rantemarioensis D.C.Thomas & Ardi, B. sanguineopilosa D.C.Thomas & Ardi, B. torajana D.C.Thomas & Ardi and B. vermeulenii D.C.Thomas, are described from South and West Sulawesi, Indonesia. All belong to Begonia section Petermannia. Proposed conservation categories for these species are Vulnerable (VU) for Begonia comestibilis, B. nobmanniae, B. prionota, B. sanguineopilosa and B. vermeulenii; Least Concern (LC) for B. lasioura, B. rantemarioensis and B. torajana; and Data Deficient (DD) for B. insueta. An identification key to Begonia in South and West Sulawesi (Sulawesi Selatan and Sulawesi Barat) is provided. © 2011 Trustees of the Royal Botanic Garden Edinburgh.published_or_final_versio

    Skeletal muscle cells possess a 'memory' of acute early life TNF-α exposure: role of epigenetic adaptation.

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    Sufficient quantity and quality of skeletal muscle is required to maintain lifespan and healthspan into older age. The concept of skeletal muscle programming/memory has been suggested to contribute to accelerated muscle decline in the elderly in association with early life stress such as fetal malnutrition. Further, muscle cells in vitro appear to remember the in vivo environments from which they are derived (e.g. cancer, obesity, type II diabetes, physical inactivity and nutrient restriction). Tumour-necrosis factor alpha (TNF-α) is a pleiotropic cytokine that is chronically elevated in sarcopenia and cancer cachexia. Higher TNF-α levels are strongly correlated with muscle loss, reduced strength and therefore morbidity and earlier mortality. We have extensively shown that TNF-α impairs regenerative capacity in mouse and human muscle derived stem cells [Meadows et al. (J Cell Physiol 183(3):330-337, 2000); Foulstone et al. (J Cell Physiol 189(2):207-215, 2001); Foulstone et al. (Exp Cell Res 294(1):223-235, 2004); Stewart et al. (J Cell Physiol 198(2):237-247, 2004); Al-Shanti et al. (Growth factors (Chur, Switzerland) 26(2):61-73, 2008); Saini et al. (Growth factors (Chur, Switzerland) 26(5):239-253, 2008); Sharples et al. (J Cell Physiol 225(1):240-250, 2010)]. We have also recently established an epigenetically mediated mechanism (SIRT1-histone deacetylase) regulating survival of myoblasts in the presence of TNF-α [Saini et al. (Exp Physiol 97(3):400-418, 2012)]. We therefore wished to extend this work in relation to muscle memory of catabolic stimuli and the potential underlying epigenetic modulation of muscle loss. To enable this aim; C2C12 myoblasts were cultured in the absence or presence of early TNF-α (early proliferative lifespan) followed by 30 population doublings in the absence of TNF-α, prior to the induction of differentiation in low serum media (LSM) in the absence or presence of late TNF-α (late proliferative lifespan). The cells that received an early plus late lifespan dose of TNF-α exhibited reduced morphological (myotube number) and biochemical (creatine kinase activity) differentiation vs. control cells that underwent the same number of proliferative divisions but only a later life encounter with TNF-α. This suggested that muscle cells had a morphological memory of the acute early lifespan TNF-α encounter. Importantly, methylation of myoD CpG islands were increased in the early TNF-α cells, 30 population doublings later, suggesting that even after an acute encounter with TNF-α, the cells have the capability of retaining elevated methylation for at least 30 cellular divisions. Despite these fascinating findings, there were no further increases in myoD methylation or changes in its gene expression when these cells were exposed to a later TNF-α dose suggesting that this was not directly responsible for the decline in differentiation observed. In conclusion, data suggest that elevated myoD methylation is retained throughout muscle cells proliferative lifespan as result of early life TNF-α treatment and has implications for the epigenetic control of muscle loss

    Use of supplementary aggregates in mortars produced using a novel lime drying technique

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    Formulated Lime mortars suitable for long-term storage in silos or bags can be produced by adding quicklime to wet, as-received quarried sand. However, sands with high water content may require the addition of so much quicklime that would alter the mortar proportioning. This work investigates the possibility to replace part of the lime-dried sand with dry crushed mixed glass cullet and calcium carbonate aggregate to allow greater control over mortar formulations. It is shown that the use of glass yields a similar or slightly weaker product, depending upon curing regime, than the control whilst calcium carbonate generates the strongest mortar

    Longevity and skeletal muscle mass: the role of IGF signalling, the sirtuins, dietary restriction and protein intake.

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    Advancing age is associated with a progressive loss of skeletal muscle (SkM) mass and function. Given the worldwide aging demographics, this is a major contributor to morbidity, escalating socio-economic costs and ultimately mortality. Previously, it has been established that a decrease in regenerative capacity in addition to SkM loss with age coincides with suppression of insulin/insulin-like growth factor signalling pathways. However, genetic or pharmacological modulations of these highly conserved pathways have been observed to significantly enhance life and healthspan in various species, including mammals. This therefore provides a controversial paradigm in which reduced regenerative capacity of skeletal muscle tissue with age potentially promotes longevity of the organism. This paradox will be assessed and considered in the light of the following: (i) the genetic knockout, overexpression and pharmacological models that induce lifespan extension (e.g. IRS-1/s6K KO, mTOR inhibition) versus the important role of these signalling pathways in SkM growth and adaptation; (ii) the role of the sirtuins (SIRTs) in longevity versus their emerging role in SkM regeneration and survival under catabolic stress; (iii) the role of dietary restriction and its impact on longevity versus skeletal muscle mass regulation; (iv) the crosstalk between cellular energy metabolism (AMPK/TSC2/SIRT1) and survival (FOXO) versus growth and repair of SkM (e.g. AMPK vs. mTOR); and (v) the impact of protein feeding in combination with dietary restriction will be discussed as a potential intervention to maintain SkM mass while increasing longevity and enabling healthy aging

    Impaired hypertrophy in myoblasts is improved with testosterone administration

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    We investigated the ability of testosterone (T) to restore differentiation in multiple population doubled (PD) murine myoblasts, previously shown to have reduced differentiation in monolayer and bioengineered skeletal muscle cultures vs. their parental controls (CON) (Sharples et al., 2011, 2012 [7] and [26]). Cells were exposed to low serum conditions in the presence or absence of T (100 nM) ± PI3K inhibitor (LY294002) for 72 h and 7 days (early and late muscle differentiation respectively). Morphological analyses were performed to determine myotube number, diameter (μm) and myonuclear accretion as indices of differentiation and myotube hypertrophy. Changes in gene expression for myogenin, mTOR and myostatin were also performed. Myotube diameter in CON and PD cells increased from 17.32 ± 2.56 μm to 21.02 ± 1.89 μm and 14.58 ± 2.66 μm to 18.29 ± 3.08 μm (P ≤ 0.05) respectively after 72 h of T exposure. The increase was comparable in both PD (+25%) and CON cells (+21%) suggesting a similar intrinsic ability to respond to exogenous T administration. T treatment also significantly increased myonuclear accretion (% of myotubes expressing 5+ nuclei) in both cell types after 7 days exposure (P ≤ 0.05). Addition of PI3K inhibitor (LY294002) in the presence of T attenuated these effects in myotube morphology (in both cell types) suggesting a role for the PI3K pathway in T stimulated hypertrophy. Finally, PD myoblasts showed reduced responsiveness to T stimulated mRNA expression of mTOR vs. CON cells and T also reduced myostatin expression in PD myoblasts only. The present study demonstrates testosterone administration improves hypertrophy in myoblasts that basally display impaired differentiation and hypertrophic capacity vs. their parental controls, the action of testosterone in this model was mediated by PI3K/Akt pathway

    AMALGAM: automatic mapping among lexicogrammatical annotation models

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    Several Corpus Linguistics research groups have gone beyond collation of 'raw' text, to syntactic annotation of the text. However, linguists developing these linguistic resources have used quite different wordtagging and parse-tree labelling schemes in each of these annotated corpora. This restricts the accessibility of each corpus, making it impossible for speech and handwriting researchers to collate them into a single very large training set. This is particularly problematic as there is evidence that one of these parsed corpora on its own is too small for a general statistical model of grammatical structure, but the combined size of all the above annotated corpora should deliver a much more reliable model. We are developing a set of mapping algorithms to map between the main tagsets and phrase structure grammar schemes used in the above corpora. We plan to develop a Multi-tagged Corpus and a MultiTreebank, a single text-set annotated with all the above tagging and parsing schemes. The text-set is the Spoken English Corpus: this is a half-way house between formal written text and colloquial conversational speech. However, the main deliverable to the computational linguistics research community is not the SEC-based MultiTreebank, but the mapping suite used to produce it - this can be used to combine currently-incompatible syntactic training sets into a large unified multicorpus. Our architecture combines standard statistical language modelling and a rule-base derived from linguists' analyses of tagset-mappings, in a novel yet intuitive way. Our development of the mapping algorithms aims to distinguish notational from substantive differences in the annotation schemes, and we will be able to evaluate tagging schemes in terms of how well they fit standard statistical language models such as n-pos (Markov) models

    L-glutamine improves skeletal muscle cell differentiation and prevents myotube atrophy after cytokine (TNF-α) stress via reduced p38 MAPK signal transduction

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    Tumour Necrosis Factor- Alpha (TNF-α) is chronically elevated in conditions where skeletal muscle loss occurs. As L-glutamine can dampen the effects of inflamed environments, we investigated the role of L-glutamine in both differentiating C2C12 myoblasts and existing myotubes in the absence/presence of TNF-α (20 ng.ml−1) ± L-glutamine (20 mM).TNF-α reduced the proportion of cells in G1 phase, as well as biochemical (CK activity) and morphological differentiation (myotube number), with corresponding reductions in transcript expression of: Myogenin, Igf-I and Igfbp5. Furthermore, when administered to mature myotubes, TNF-α induced myotube loss and atrophy underpinned by reductions in Myogenin, Igf-I, Igfbp2 and glutamine synthetase and parallel increases in Fox03, Cfos, p53 and Bid gene expression. Investigation of signaling activity suggested that Akt and ERK1/2 were unchanged, JNK increased (non-significantly) whereas P38 MAPK substantially and significantly increased in both myoblasts and myotubes in the presence of TNF-α. Importantly, 20 mM L-glutamine reduced p38 MAPK activity in TNF-α conditions back to control levels, with a corresponding rescue of myoblast differentiation and a reversal of atrophy in myotubes. L-glutamine resulted in upregulation of genes associated with growth and survival including; Myogenin, Igf-Ir, Myhc2 & 7, Tnfsfr1b, Adra1d and restored atrophic gene expression of Fox03 back to baseline in TNF-α conditions. In conclusion, L-glutamine supplementation rescued suppressed muscle cell differentiation and prevented myotube atrophy in an inflamed environment via regulation of p38 MAPK. L-glutamine administration could represent an important therapeutic strategy for reducing muscle loss in catabolic diseases and inflamed ageing. This article is protected by copyright. All rights reserve
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