29 research outputs found
High-redshift star formation rate up to z~8.3 derived from gamma-ray bursts and influence of background cosmology
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 CDM, quintessence, quintessence with a
time-varying equation of state, and brane-world model. We use latest Swift GRBs
including two highest- GRBs, GRB 080913 at and GRB 090423 at
. We find that the SFR at shows a steep decay with a slope of
in CDM. In the other three models, the high-redshift SFR
is slightly different from CDM 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
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
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
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