992 resultados para twisted canonical homomorphism


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We define and prove the existence of free Banach lattices in the category of Banach lattices and contractive lattice homomorphisms, and establish some of their fundamental properties. We give much more detailed results about their structure in the case when there are only a finite number of generators, and give several Banach lattice characterizations of the number of generators being, respectively, one, finite or countable. We define a Banach lattice P to be projective if, whenever X is a Banach lattice, J is a closed ideal in X, Q : X → X/J is the quotient map, T: P → X/J is a linear lattice homomorphism and ε > 0, there exists a linear lattice homomorphism : P → X such thatT = Q º and ∥∥ ≤ (1 + ε)∥T∥. We establish the connection between projective Banach lattices and free Banach lattices, describe several families of Banach lattices that are projective and prove that some are not.

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Four different bombesins (bombesin, His(6)-bombesin, Phe(13)-bombesin and Asp(2)-, Phe(4)-SAP-bombesin) have been identified by a systematic sequencing study of peptides in reverse phase HPLC fractions of the skin secretion of the European yellow-bellied toad, Bombina variegata, that had been solvated in 0.1% (v/v) aqueous trifluoroacetic acid (TFA) and stored frozen at -20°C for 12 years. By using a 3'- and 5'-RACE PCR strategy, the corresponding biosynthetic precursor-encoding cDNAs of all four peptides were cloned from a cDNA library made from the same long-term frozen, acid-solvated skin secretion sample following thawing and lyophilization. Canonical bombesin and His(6)-bombesin are classical bombesin sub-family members, whereas Phe(13)-bombesin and Asp(2)-, Phe(4)-SAP-bombesin, belong to the litorin/ranatensin sub-family of bombesin-like peptides (BLPs). Assignment of these peptides to respective sub-families, was based upon both their primary structural similarities and their comparative pharmacological activities. An interesting observation in this study, was that the nucleotide sequences of the open-reading frames of cloned cDNAs encoding bombesin and its His(6)-substituted analog, were identical except for a single base that was responsible for the change observed at the position 6 residue in the mature peptide from Asn to His. In contrast, the precursor cDNA nucleotide sequences encoding the Phe(13)-bombesins, exhibited 53 base differences. The pharmacological activities of synthetic replicates of each bombesin were compared using two different mammalian smooth muscle preparations and all four peptides were found to be active. However, there were significant differences in their relative potencies.

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Elafin is a 6-kDa innate immune protein present at several epithelial surfaces including the pulmonary epithelium. It is a canonical protease inhibitor of two neutrophil serine proteases [neutrophil elastase (NE) and proteinase 3] with the capacity to covalently bind extracellular matrix proteins by transglutamination. In addition to these properties, elafin also possesses antimicrobial and immunomodulatory activities. The aim of the present study was to investigate the effect of Pseudomonas aeruginosa proteases on elafin function. We found that P aeruginosa PAO1-conditioned medium and two purified Pseudomonas metalloproteases, pseudolysin (elastase) and aeruginolysin (alkaline protease), are able to cleave recombinant elafin. Pseudolysin was shown to inactivate the anti-NE activity of elafin by cleaving its protease-binding loop. Interestingly, antibacterial properties of elafin against PAO1 were found to be unaffected after pseudolysin treatment. In contrast to pseudolysin, aeruginolysin failed to inactivate the inhibitory properties of elafin against NE. Aeruginolysin cleaves elafin at the amino-terminal Lys6-Gly7 peptide bond, resulting in a decreased ability to covalently bind purified fibronectin following transglutaminase activity. In conclusion, this study provides evidence that elafin is susceptible to proteolytic cleavage at alternative sites by P aeruginosa metalloproteinases, which can affect different biological functions of elafin.

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Naphthalenic compounds are a rich resource for designers of fluorescent sensing/switching/logic systems. The degree of internal charge transfer (ICT) character in the fluorophore excited states can vary from negligible to substantial. Naphthalene-1,8;4,5-diimides (11–13), 1,8-naphthalimides (16) and 4-chloro-1,8-naphthalimides (15) are of the former type. The latter type is represented by the 4-alkylamino-1,8-naphthalimides (1). Whether ICT-based or not, these serve as the fluorophore in ‘fluorophore-spacer-receptor’ switching systems where PET holds sway until the receptor is bound to H+. On the other hand, 4-dialkylamino-1,8-naphthalimides (3–4) show modest H+-induced fluorescence switching unless the 4-dialkylamino group is a part of a small ring (5). Electrostatic destabilization of a non-emissive twisted internal charge transfer (ICT) excited state is the origin of this behaviour. An evolution to the non-emissive twisted ICT excited state is responsible for the weak emission of the model compound 6 (and related structures 7 and 8) across the pH range. Twisted ICT excited states are also implicated in the switch 9 and its model compound 10, which are based on the 6-dialkylamino-3H-benzimidazo[2,1-a]benz[d,e]isoquinolin-3-one fluorophore.

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We investigate the brightness distribution expected for thermonuclear explosions that might result from the ignition of a detonation during the violent merger of white dwarf (WD) binaries. Violent WD mergers are a subclass of the canonical double degenerate scenario where two carbon-oxygen (CO) WDs merge when the larger WD fills its Roche lobe. Determining their brightness distribution is critical for evaluating whether such an explosion model could be responsible for a significant fraction of the observed population of Type Ia supernovae (SNe Ia). We argue that the brightness of an explosion realized via the violent merger model is mainly determined by the mass of Ni produced in the detonation of the primary COWD. To quantify this link, we use a set of sub-Chandrasekhar mass WD detonation models to derive a relationship between primary WD mass (m) and expected peak bolometric brightness (M). We use this m-M relationship to convert the masses of merging primary WDs from binary population models to a predicted distribution of explosion brightness. We also investigate the sensitivity of our results to assumptions about the conditions required to realize a detonation during violent mergers ofWDs. We find a striking similarity between the shape of our theoretical peak-magnitude distribution and that observed for SNe Ia: our model produces a M distribution that roughly covers the range and matches the shape of the one observed for SNe Ia. However, this agreement hinges on a particular phase of mass accretion during binary evolution: the primary WD gains ~0.15-0.35M? from a slightly evolved helium star companion. In our standard binary evolution model, such an accretion phase is predicted to occur for about 43 per cent of all binary systems that ultimately give rise to binary CO WD mergers. We also find that with high probability, violent WD mergers involving the most massive primaries (?1.3M?, which should produce bright SNe) have delay times ?500 Myr. © 2012 The Authors. Published by Oxford University Press on behalf of the Royal Astronomical Society.

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Thecamoebians were examined from 123 surface sediment samples collected from 45 lakes in the Greater Toronto Area (GTA) and the surrounding region to i) elucidate the controls on faunal distribution in modern lake environments; and ii) to consider the utility of thecamoebians in quantitative studies of water quality change. This area was chosen because it includes a high density of lakes that are threatened by urban development and where water quality has deteriorated locally as a result of contaminant inputs, particularly nutrients. Canonical Correspondence analysis (CCA) and a series of partial CCAs were used to examine species-environment relationships. Twenty-four environmental variables were considered, including water properties (e.g. pH, DO, conductivity), substrate characteristics, nutrient loading, and environmentally available metals. The thecamoebian assemblages showed a strong association with Olsen's Phosphorus, reflecting the eutrophic status of many of the lakes, and locally to elevated conductivity measurements, which appear to reflect road salt inputs associated with winter de-icing operations. A transfer function was developed for Olsen P using this training set based on weighted averaging with inverse deshrinking (WA Inv). The model was applied to infer past changes in Phosphorus enrichment in core samples from several lakes, including eutrophic Haynes Lake within the GTA. Thecamoebian-inferred changes in sedimentary Phosphorus from a 210Pb dated core from Haynes Lake are related to i) widespread introduction of chemical fertilizers to agricultural land in the post WWII era; ii) a steep decline in Phosphorous with a change in agricultural practices in the late 1970s; and iii) the construction of a golf course in close proximity to the lake in the early 1990s. This preliminary study confirms that thecamoebians have considerable potential as indicators of eutrophication in lakes and can provide an estimate of baseline conditions.

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MicroRNAs (miRNAs) are single-stranded non-coding RNAs that negatively regulate target gene expression through mRNA cleavage or translational repression. There is mounting evidence that they play critical roles in heart disease. The expression of known miRNAs in the heart has been studied at length by microarray and quantitative PCR but it is becoming evident that microRNA isoforms (isomiRs) are potentially physiologically important. It is well known that left ventricular (patho)physiology is influenced by transmural heterogeneity of cardiomyocyte phenotype, and this likely reflects underlying heterogeneity of gene expression. Given the significant role of miRNAs in regulating gene expression, knowledge of how the miRNA profile varies across the ventricular wall will be crucial to better understand the mechanisms governing transmural physiological heterogeneity. To determinine miRNA/isomiR expression profiles in the rat heart we investigated tissue from different locations across the left ventricular wall using deep sequencing. We detected significant quantities of 145 known rat miRNAs and 68 potential novel orthologs of known miRNAs, in mature, mature* and isomiR formation. Many isomiRs were detected at a higher frequency than their canonical sequence in miRBase and have different predicted targets. The most common miR-133a isomiR was more effective at targeting a construct containing a sequence from the gelsolin gene than was canonical miR-133a, as determined by dual-fluorescence assay. We identified a novel rat miR-1 homolog from a second miR-1 gene; and a novel rat miRNA similar to miR-676. We also cloned and sequenced the rat miR-486 gene which is not in miRBase (v18). Signalling pathways predicted to be targeted by the most highly detected miRNAs include Ubiquitin-mediated Proteolysis, Mitogen-Activated Protein Kinase, Regulation of Actin Cytoskeleton, Wnt signalling, Calcium Signalling, Gap junctions and Arrhythmogenic Right Ventricular Cardiomyopathy. Most miRNAs are not expressed in a gradient across the ventricular wall, with exceptions including miR-10b, miR-21, miR-99b and miR-486.

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Concentrations of major ions, silicate and nutrients (total N and P) were measured in samples of surface water from 28 lakes in ice-free areas of northern Victoria Land (East Antarctica). Sixteen lakes were sampled during austral summers 2001/02, 2003/04, 2004/05 and 2005/06 to assess temporal variation in water chemistry. Although samples showed a wide range in ion concentrations, their composition mainly reflected that of seawater. In general, as the distance from the sea increased, the input of elements from the marine environment (through aerosols and seabirds) decreased and there was an increase in nitrate and sulfate concentrations. Antarctic lakes lack outflows and during the austral summer the melting and/or ablation of ice cover, water evaporation and leaching processes in dry soils determine a progressive increase in water ion concentrations. During the five-year monitoring survey, no statistically significant variation in the water chemistry were detected, except for a slight (hardly significant) increase in TN concentrations. However, Canonical Correspondence Analysis (CCA) indicated that other factors besides distance from the sea, the presence of nesting seabirds, the sampling time and percentage of ice cover affect the composition of water in Antarctic cold desert environments.

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We perform an extensive study of the properties of global quantum correlations in finite-size one-dimensional quantum spin models at finite temperature. By adopting a recently proposed measure for global quantum correlations (Rulli and Sarandy 2011 Phys. Rev. A 84 042109), called global discord, we show that critical points can be neatly detected even for many-body systems that are not in their ground state. We consider the transverse Ising model, the cluster-Ising model where three-body couplings compete with an Ising-like interaction, and the nearest-neighbor XX Hamiltonian in transverse magnetic field. These models embody our canonical examples showing the sensitivity of global quantum discord close to criticality. For the Ising model, we find a universal scaling of global discord with the critical exponents pertaining to the Ising universality class.

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Although Wnt signaling is known to mediate multiple biological and pathological processes, its association with diabetic retinopathy (DR) has not been established. Here we show that retinal levels and nuclear translocation of beta-catenin, a key effector in the canonical Wnt pathway, were increased in humans with DR and in three DR models. Retinal levels of low-density lipoprotein receptor-related proteins 5 and 6, coreceptors of Wnts, were also elevated in the DR models. The high glucose-induced activation of beta-catenin was attenuated by aminoguanidine, suggesting that oxidative stress is a direct cause for the Wnt pathway activation in diabetes. Indeed, Dickkopf homolog 1, a specific inhibitor of the Wnt pathway, ameliorated retinal inflammation, vascular leakage, and retinal neovascularization in the DR models. Dickkopf homolog 1 also blocked the generation of reactive oxygen species induced by high glucose, suggesting that Wnt signaling contributes to the oxidative stress in diabetes. These observations indicate that the Wnt pathway plays a pathogenic role in DR and represents a novel therapeutic target.

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Small RNA-mediated chromatin silencing is well characterized for repeated sequences and transposons, but its role in regulating single-copy endogenous genes is unclear. We have identified two small RNAs (30 and 24 nucleotides) corresponding to the reverse strand 3' to the canonical poly(A) site of FLOWERING LOCUS C (FLC), an Arabidopsis gene encoding a repressor of flowering. Genome searches suggest that these RNAs originate from the FLC locus in a genomic region lacking repeats. The 24-nt small RNA, which is most abundant in developing fruits, is absent in mutants defective in RNA polymerase IVa, RNA-DEPENDENT RNA POLYMERASE 2, and DICER-LIKE 3, components required for RNAi-mediated chromatin silencing. The corresponding genomic region shows histone 3 lysine 9 dimethylation, which was reduced in a dcl2,3,4 triple mutant. Investigations into the origins of the small RNAs revealed a polymerase IVa-dependent spliced, antisense transcript covering the 3' FLC region. Mutation of this genomic region by T-DNA insertion led to FLC misexpression and delayed flowering, suggesting that RNAi-mediated chromatin modification is an important component of endogenous pathways that function to suppress FLC expression.

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In eight European study sites (in Spain, Ireland, Netherlands, Germany, Poland, Estonia and Sweden), abundance of breeding farmland bird territories was obtained from 500 × 500 m survey plots (30 per area, N = 240) using the mapping method. Two analyses were performed: (I) a Canonical Correspondence Analysis of species abundance in relation to geographical location and variables measuring agricultural intensification at field and farm level to identify significant intensification variables and to estimate the fractions of total variance in bird abundance explained by geography and agricultural intensification; (II) several taxonomic and functional community indices were built and analysed using GLM in relation to the intensification variables found significant in the CCA. The geographical location of study sites alone explains nearly one fifth (19. 5%) of total variation in species abundance. The fraction of variance explained by agricultural intensification alone is much smaller (4. 3%), although significant. The intersection explains nearly two fifths (37. 8%) of variance in species abundance. Community indices are negatively affected by correlates of intensification like farm size and yield, whereas correlates of habitat availability and quality have positive effects on taxonomic and functional diversity of assemblages. Most of the purely geographical variation in farmland bird assemblage composition is associated to Mediterranean steppe species, reflecting the bio-geographical singularity of that assemblage and reinforcing the need to preserve this community. Taxonomic and functional diversity of farmland bird communities are negatively affected by agricultural intensification and positively affected by increasing farmland habitat availability and quality. © 2011 Springer Science+Business Media B.V.

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Deregulated NOTCH1 has been reported in lymphoid leukaemia, although its role in chronic myeloid leukaemia (CML) is not well established. We previously reported BCR-ABL down-regulation of a novel haematopoietic regulator, CCN3, in CML; CCN3 is a non-canonical NOTCH1 ligand. This study characterizes the NOTCH1–CCN3 signalling axis in CML. In K562 cells, BCR-ABL silencing reduced full-length NOTCH1 (NOTCH1-FL) and inhibited the cleavage of NOTCH1 intracellular domain (NOTCH1-ICD), resulting in decreased expression of the NOTCH1 targets c-MYC and HES1. K562 cells stably overexpressing CCN3 (K562/CCN3) or treated with recombinant CCN3 (rCCN3) showed a significant reduction in NOTCH1 signalling (> 50% reduction in NOTCH1-ICD, p < 0.05). Gamma secretase inhibitor (GSI), which blocks NOTCH1 signalling, reduced K562/CCN3 colony formation but increased that of K562/control cells. GSI combined with either rCCN3 or imatinib reduced K562 colony formation with enhanced reduction of NOTCH1 signalling observed with combination treatments. We demonstrate an oncogenic role for NOTCH1 in CML and suggest that BCR-ABL disruption of NOTCH1–CCN3 signalling contributes to the pathogenesis of CML.

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Objective: Vascular lineage differentiation of stem/progenitor cells can contribute to both tissue repair and exacerbation of vascular diseases such as in vein grafts. The role of macrophages in controlling vascular progenitor differentiation is largely unknown and may play an important role in graft development. This study aims to identify the role of macrophages in vascular stem/progenitor cell differentiation and thereafter elucidate the mechanisms that are involved in the macrophage- mediated process.

Approach and Results: We provide in vitro evidence that macrophages can induce endothelial cell (EC) differentiation of the stem/progenitor cells while simultaneously inhibiting their smooth muscle cell differentiation. Mechanistically, both effects were mediated by macrophage-derived tumor necrosis factor-α (TNF-α) via TNF-α receptor 1 and canonical nuclear factor-κB activation. Although the overexpression of p65 enhanced EC (or attenuated smooth muscle cell) differentiation, p65 or TNF-α receptor 1 knockdown using lentiviral short hairpin RNA inhibited EC (or rescued smooth muscle cell) differentiation in response to TNF-α. Furthermore, TNF-α–mediated EC differentiation was driven by direct binding of nuclear factor-κB (p65) to specific VE-cadherin promoter sequences. Subsequent experiments using an ex vivo decellularized vessel scaffold confirmed an increase in the number of ECs and reduction in smooth muscle cell marker expression in the presence of TNF-α. The lack of TNF-α in a knockout mouse model of vein graft decreased endothelialization and significantly increased thrombosis formation.

Conclusions: Our study highlights the role of macrophages in directing vascular stem/progenitor cell lineage commitment through TNF-α–mediated TNF-α receptor 1 and nuclear factor-κB activation that is likely required for endothelial repair in vascular diseases such as vein graft.

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In 1976, Susan Brownmiller published 'Against Our Will', widely credited as the founding text of feminist anti-rape theory, in which she famously declared that rape was 'nothing more or less than a conscious process of intimidation by which all men keep all women in a state of fear'.While the scholarship and politics of Against Our Will have been subjected to numerous and compelling critiques, the work retains canonical and even foundational status within feminist anti-rape politics. In this article I attempt a critical re-examination of feminist (her)story telling practices. By situating the story told in Against Our Will beside and within Brownmiller's story of the creation of the book and her own coming-to-consciousness, a more general reexamination of the role of women's speech and (her)story-telling in feminist anti-rape politics is afforded. This re-reading draws out two central aspects of the politics of (her)story-telling which can be found in Brownmiller's work and in the Joan W. Scott quotation above. Firstly, the need to be recognised as a 'just source' of women's stories has resulted in the granting of epistemological primacy to stories of women's experience or personal statements. Secondly, the desire to compensate for the lack of a 'classical myth' to authorise women's claims, resulting in an attempt to imbue these feminist (her)stories with their own mythology.