29 research outputs found

    High-redshift star formation rate up to z~8.3 derived from gamma-ray bursts and influence of background cosmology

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    The high-redshift star formation rate (SFR) is difficult to measure directly even by modern approaches. Long-duration gamma-ray bursts (GRBs) can be detected to the edge of the visible universe because of their high luminorsities. The collapsar model of long gamma-ray bursts indicates that they may trace the star formation history. So long gamma-ray bursts may be a useful tool of measuring the high-redshift SFR. Observations show that long gamma-ray bursts prefer to form in a low-metallicity environment. We study the high-redshift SFR up to z~8.3 considering the Swift GRBs tracing the star formation history and the cosmic metallicity evolution in different background cosmological models including Λ\LambdaCDM, quintessence, quintessence with a time-varying equation of state, and brane-world model. We use latest Swift GRBs including two highest-zz GRBs, GRB 080913 at z=6.7z=6.7 and GRB 090423 at z=8.3z=8.3. We find that the SFR at z>4z>4 shows a steep decay with a slope of ∼−5.0\sim -5.0 in Λ\LambdaCDM. In the other three models, the high-redshift SFR is slightly different from Λ\LambdaCDM model, and also shows a steep decay.Comment: 5 pages, 5 figures, 2 tables, two references adde

    GeV Gamma-Ray Attenuation and the High-Redshift UV Background

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    We present new calculations of the evolving UV background out to the epoch of cosmological reionization and make predictions for the amount of GeV gamma-ray attenuation by electron-positron pair production. Our results are based on recent semi-analytic models of galaxy formation, which provide predictions of the dust-extinguished UV radiation field due to starlight, and empirical estimates of the contribution due to quasars. We account for the reprocessing of ionizing photons by the intergalactic medium. We test whether our models can reproduce estimates of the ionizing background at high redshift from flux decrement analysis and proximity effect measurements from quasar spectra, and identify a range of models that can satisfy these constraints. Pair-production against soft diffuse photons leads to a spectral cutoff feature for gamma rays observed between 10 and 100 GeV. This cutoff varies with redshift and the assumed star formation and quasar evolution models. We find only negligible amounts of absorption for gamma rays observed below 10 GeV for any emission redshift. With observations of high-redshift sources in sufficient numbers by the Fermi Gamma-ray Space Telescope and new ground-based instruments it should be possible to constrain the extragalactic background light in the UV and optical portion of the spectrum.Comment: 19 pages, 12 figures, Accepted for publication in MNRAS, this version includes minor correction

    Protein deamidation

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    A completely automatic computerized technique for the quantitative estimation of the deamidation rates of any protein for which the three-dimensional structure is known has been developed. Calculations of the specific deamidation rates of 170,014 asparaginyl residues in 13,335 proteins have been carried out. The calculated values have good quantitative reliability when compared with experimental measurements. These rates demonstrate that deamidation may be a biologically relevant phenomenon in a remarkably large percentage of proteins

    Cell surface expression of an endoplasmic reticulum resident heat shock protein gp96 triggers MyD88-dependent systemic autoimmune diseases

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    Heat shock proteins have been implicated as endogenous activators for dendritic cells (DCs). Without tissue distress or death, these intracellular molecules are inaccessible to surface receptor(s) on DCs, possibly to avoid uncontrolled DC activation and breakdown of immunologic tolerance. We herein addressed this hypothesis in transgenic mice by enforcing cell surface expression of gp96, a ubiquitous heat shock protein of the endoplasmic reticulum. Although a pan-specific promoter is used for transgene expression, neither the expression level nor the tissue distribution of the endogenous gp96 was altered by this maneuver. However, cell surface gp96 induced significant DC activations and spontaneous lupus-like autoimmune diseases, even though the development/functions of lymphocytic compartments were unaltered. Using a bone marrow chimera approach, we further demonstrated that both DC activation and autoimmunity elicited by cell surface gp96 are dependent on the downstream adaptor protein MyD88 for signaling by Toll/IL-1 receptor family. Our study not only established the proinflammatory property of cell surface gp96 in vivo, but also suggested a chronic stimulation of DCs by gp96 as a pathway to initiate spontaneous autoimmune diseases
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