631 research outputs found

    Type Ia supernova Hubble diagram with near-infrared and optical observations

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    We main goal of this paper is to test whether the NIR peak magnitudes of SNe Ia could be accurately estimated with only a single observation obtained close to maximum light, provided the time of B band maximum and the optical stretch parameter are known. We obtained multi-epoch UBVRI and single-epoch J and H photometric observations of 16 SNe Ia in the redshift range z=0.037-0.183, doubling the leverage of the current SN Ia NIR Hubble diagram and the number of SNe beyond redshift 0.04. This sample was analyzed together with 102 NIR and 458 optical light curves (LCs) of normal SNe Ia from the literature. The analysis of 45 well-sampled NIR LCs shows that a single template accurately describes them if its time axis is stretched with the optical stretch parameter. This allows us to estimate the NIR peak magnitudes even with one observation obtained within 10 days from B-band maximum. We find that the NIR Hubble residuals show weak correlation with DM_15 and E(B-V), and for the first time we report a possible dependence on the J_max-H_max color. The intrinsic NIR luminosity scatter of SNe Ia is estimated to be around 0.10 mag, which is smaller than what can be derived for a similarly heterogeneous sample at optical wavelengths. In conclusion, we find that SNe Ia are at least as good standard candles in the NIR as in the optical. We showed that it is feasible to extended the NIR SN Ia Hubble diagram to z=0.2 with very modest sampling of the NIR LCs, if complemented by well-sampled optical LCs. Our results suggest that the most efficient way to extend the NIR Hubble diagram to high redshift would be to obtain a single observation close to the NIR maximum. (abridged)Comment: 39 pages, 15 figures, accepted by A&

    NEW SEISMIC SOURCE ZONE MODEL FOR PORTUGAL AND AZORES

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    The development of seismogenic source models is one of the first steps in seismic hazard assessment. In seismic hazard terminology, seismic source zones (SSZ) are polygons (or volumes) that delineate areas with homogeneous characteristics of seismicity. The importance of using knowledge on geology, seismicity and tectonics in the definition of source zones has been recognized for a long time [1]. However, the definition of SSZ tends to be subjective and controversial. Using SSZ based on broad geology, by spreading the seismicity clusters throughout the areal extent of a zone, provides a way to account for possible long-term non-stationary seismicity behavior [2,3]. This approach effectively increases seismicity rates in regions with no significant historical or instrumental seismicity, while decreasing seismicity rates in regions that display higher rates of seismicity. In contrast, the use of SSZ based on concentrations of seismicity or spatial smoothing results in stationary behavior [4]. In the FP7 Project SHARE (Seismic Hazard Harmonization in Europe), seismic hazard will be assessed with a logic tree approach that allows for three types of branches for seismicity models: a) smoothed seismicity, b) SSZ, c) SSZ and faults. In this context, a large-scale zonation model for use in the smoothed seismicity branch, and a new consensus SSZ model for Portugal and Azores have been developed. The new models were achieved with the participation of regional experts by combining and adapting existing models and incorporating new regional knowledge of the earthquake potential. The main criteria used for delineating the SSZ include distribution of seismicity, broad geological architecture, crustal characteristics (oceanic versus continental, tectonically active versus stable, etc.), historical catalogue completeness, and the characteristics of active or potentially-active faults. This model will be integrated into an Iberian model of SSZ to be used in the Project SHARE seismic hazard assessment

    COMPILATION OF ACTIVE FAULT DATA IN PORTUGAL FOR USE IN SEISMIC HAZARD ANALYSIS

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    To estimate where future earthquakes are likely to occur, it is essential to combine information about past earthquakes with knowledge about the location and seismogenic properties of active faults. For this reason, robust probabilistic seismic hazard analysis (PSHA) integrates seismicity and active fault data. Existing seismic hazard assessments for Portugal rely exclusively on seismicity data and do not incorporate data on active faults. Project SHARE (Seismic Hazard Harmonization in Europe) is an EC-funded initiative (FP7) that aims to evaluate European seismic hazards using an integrated, standardized approach. In the context of SHARE, we are developing a fully-parameterized active fault database for Portugal that incorporates existing compilations, updated according to the most recent publications. The seismogenic source model derived for SHARE will be the first model for Portugal to include fault data and follow an internationally standardized approach. This model can be used to improve both seismic hazard and risk analyses and will be combined with the Spanish database for use in Iberian- and European-scale assessments

    Evolutionary instability of Zero Determinant strategies demonstrates that winning isn't everything

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    Zero Determinant (ZD) strategies are a new class of probabilistic and conditional strategies that are able to unilaterally set the expected payoff of an opponent in iterated plays of the Prisoner's Dilemma irrespective of the opponent's strategy, or else to set the ratio between a ZD player's and their opponent's expected payoff. Here we show that while ZD strategies are weakly dominant, they are not evolutionarily stable and will instead evolve into less coercive strategies. We show that ZD strategies with an informational advantage over other players that allows them to recognize other ZD strategies can be evolutionarily stable (and able to exploit other players). However, such an advantage is bound to be short-lived as opposing strategies evolve to counteract the recognition.Comment: 14 pages, 4 figures. Change in title (again!) to comply with Nature Communications requirements. To appear in Nature Communication

    Signatures of photon and axion-like particle mixing in the gamma-ray burst jet

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    Photons couple to Axion-Like Particles (ALPs) or more generally to any pseudo Nambu-Goldstone boson in the presence of an external electromagnetic field. Mixing between photons and ALPs in the strong magnetic field of a Gamma-Ray Burst (GRB) jet during the prompt emission phase can leave observable imprints on the gamma-ray polarization and spectrum. Mixing in the intergalactic medium is not expected to modify these signatures for ALP mass > 10^(-14) eV and/or for < nG magnetic field. We show that the depletion of photons due to conversion to ALPs changes the linear degree of polarization from the values predicted by the synchrotron model of gamma ray emission. We also show that when the magnetic field orientation in the propagation region is perpendicular to the field orientation in the production region, the observed synchrotron spectrum becomes steeper than the theoretical prediction and as detected in a sizable fraction of GRB sample. Detection of the correlated polarization and spectral signatures from these steep-spectrum GRBs by gamma-ray polarimeters can be a very powerful probe to discover ALPs. Measurement of gamma-ray polarization from GRBs in general, with high statistics, can also be useful to search for ALPs.Comment: 17 pages, 3 figures. Accepted for publication in JCAP with minor change

    Rising Rates of All Types of Diabetes in South Asian and Non-South Asian Children and Young People Aged 0–29 Years in West Yorkshire, U.K., 1991–2006

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    OBJECTIVE: To investigate incidence trends of all diabetes types in all children and young people and in the south Asian subpopulation. RESEARCH DESIGN AND METHODS: Annual incidence per 100,000 and time trends (1991-2006) were analyzed for 2,889 individuals aged 0-29 years diagnosed with diabetes while resident in West Yorkshire, U.K. RESULTS: Diagnoses comprised type 1 (83%), type 2 (12%), maturity-onset diabetes of the young (0.7%), "J"-type/other (0.1%), and uncertain/unclassified (4%). There was a lower incidence of type 1 and a threefold excess of type 2 in south Asians compared with non-south Asians. Type 1 incidence leveled out and type 2 increased after the first south Asian case of type 2 was diagnosed in 1999. Type 2 and unclassified diabetes incidence rose in all population subgroups. CONCLUSIONS: The burden of diabetes increased over time for both ethnic groups, with a significant excess of type 2 diabetes in south Asians. The rising incidence of type 1 diabetes in south Asians attenuated as type 2 diabetes increased after 1999

    Compilation of parameterized seismogenic sources in Iberia for the SHARE European-scale seismic source model.

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    Abstract: SHARE (Seismic Hazard Harmonization in Europe) is an EC-funded project (FP7) that aims to evaluate European seismic hazards using an integrated, standardized approach. In the context of SHARE, we are compiling a fully-parameterized active fault database for Iberia and the nearby offshore region. The principal goal of this initiative is for fault sources in the Iberian region to be represented in SHARE and incorporated into the source model that will be used to produce seismic hazard maps at the European scale. The SHARE project relies heavily on input from many regional experts throughout the Euro-Mediterranean region. At the SHARE regional meeting for Iberia, the 2010 Working Group on Iberian Seismogenic Sources (WGISS) was established; these researchers are contributing to this large effort by providing their data to the Iberian regional integrators in a standardized format. The development of the SHARE Iberian active fault database is occurring in parallel with IBERFAULT, another ongoing effort to compile a database of active faults in the Iberian region. The SHARE Iberian active fault database synthesizes a wide range of geological and geophysical observations on active seismogenic sources, and incorporates existing compilations (e.g., Cabral, 1995; Silva et al., 2008), original data contributed directly from researchers, data compiled from the literature, parameters estimated using empirical and analytical relationships, and, where necessary, parameters derived using expert judgment. The Iberian seismogenic source model derived for SHARE will be the first regional-scale source model for Iberia that includes fault data and follows an internationally standardized approach (Basili et al., 2008; 2009). This model can be used in both seismic hazard and risk analyses and will be appropriate for use in Iberian- and European-scale assessments

    Platelet-derived growth factor receptor-β, carrying the activating mutation D849N, accelerates the establishment of B16 melanoma

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    <p>Abstract</p> <p>Background</p> <p>Platelet-derived growth factor (PDGF)-BB and PDGF receptor (PDGFR)-β are mainly expressed in the developing vasculature, where PDGF-BB is produced by endothelial cells and PDGFR-β is expressed by mural cells, including pericytes. PDGF-BB is produced by most types of solid tumors, and PDGF receptor signaling participates in various processes, including autocrine stimulation of tumor cell growth, recruitment of tumor stroma fibroblasts, and stimulation of tumor angiogenesis. Furthermore, PDGF-BB-producing tumors are characterized by increased pericyte abundance and accelerated tumor growth. Thus, there is a growing interest in the development of tumor treatment strategies by blocking PDGF/PDGFR function. We have recently generated a mouse model carrying an activated PDGFR-β by replacing the highly conserved aspartic acid residue (D) 849 in the activating loop with asparagine (N). This allowed us to investigate, in an orthotopic tumor model, the role of increased stromal PDGFR-β signaling in tumor-stroma interactions.</p> <p>Methods</p> <p>B16 melanoma cells lacking PDGFR-β expression and either mock-transfected or engineered to express PDGF-BB, were injected alone or in combination with matrigel into mice carrying the activated PDGFR-β (D849N) and into wild type mice. The tumor growth rate was followed and the vessel status of tumors, i.e. total vessel area/tumor, average vessel surface and pericyte density of vessels, was analyzed after resection.</p> <p>Results</p> <p>Tumors grown in mice carrying an activated PDGFR-β were established earlier than those in wild-type mice. In this early phase, the total vessel area and the average vessel surface were higher in tumors grown in mice carrying the activated PDGFR-β (D849N) compared to wild-type mice, whereas we did not find a significant difference in the number of tumor vessels and the pericyte abundance around tumor vessels between wild type and mutant mice. At later phases of tumor progression, no significant difference in tumor growth rate was observed between wild type mice and mutant mice, although the pericyte coverage was higher around tumor vessels from mutant mice.</p> <p>Conclusion</p> <p>Our findings suggest that the activated PDGFR-β (D849N) in the host animal increased the total vessel area and the average vessel surface even in PDGF-negative tumors, resulting in a shorter lag phase during tumor establishment.</p

    Cover to Volume 3

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    The fibroblast mitogen platelet-derived growth factor -BB (PDGF-BB) induces a transient expression of the orphan nuclear receptor NR4A1 (also named Nur77, TR3 or NGFIB). The aim of the present study was to investigate the pathways through which NR4A1 is induced by PDGF-BB and its functional role. We demonstrate that in PDGF-BB stimulated NIH3T3 cells, the MEK1/2 inhibitor CI-1040 strongly represses NR4A1 expression, whereas Erk5 downregulation delays the expression, but does not block it. Moreover, we report that treatment with the NF-κB inhibitor BAY11-7082 suppresses NR4A1 mRNA and protein expression. The majority of NR4A1 in NIH3T3 was found to be localized in the cytoplasm and only a fraction was translocated to the nucleus after continued PDGF-BB treatment. Silencing NR4A1 slightly increased the proliferation rate of NIH3T3 cells; however, it did not affect the chemotactic or survival abilities conferred by PDGF-BB. Moreover, overexpression of NR4A1 promoted anchorage-independent growth of NIH3T3 cells and the glioblastoma cell lines U-105MG and U-251MG. Thus, whereas NR4A1, induced by PDGF-BB, suppresses cell growth on a solid surface, it increases anchorage-independent growth
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