Cosmological Aspects of Gamma-Ray Bursts: Luminosity Evolution and an Estimate of the Star Formation Rate at High Redshifts

Using 220 Gamma-Ray Burst (GRB) redshifts and luminosities derived from the luminosity-variability relationship of Fenimore & Ramirez-Ruiz (2000), we show that there exists a significant correlation between the GRB luminosity and redshift. In particular, we find that the evolution of the average luminosity can be parameterized as L ~ (1+z)^(1.4 +- 0.5), where z is the burst redshift. We discuss the possible reasons behind this evolution and compare it to other known sources that exhibit similar behavior. In addition, we use non-parametric statistical techniques to independently estimate the distributions of the luminosity and redshift of bursts, accounting for the evolution (in contrast to previous studies which have assumed that the luminosity function is independent of redshift). We present these distributions and discuss their implications. Most significantly, we find a co-moving rate density of GRBs that continues to increase to (1+z) ~ 10. From this estimate of the GRB rate density, we then use the population synthesis codes of Fryer et al. (1999) to estimate the star formation rate at high redshifts, based on different progenitor models of GRBs. We find that no matter what the progenitor or population synthesis model, the star formation rate increases or remains constant to very high redshifts (z ~ 10).Comment: Final version accepted to the Astrophysical Journa

Star formation in quasar hosts and the origin of radio emission in radio-quiet quasars

This article has been accepted for publication in Monthly Notices of the Royal Astronomical Society following peer review. The version of record [Nadia L. Zakamska, et al., 'Star formation in quasar hosts and the origin of radio emission in radio-quiet quasars', MNRAS, 455(4): 4191-4211, first published online December 4, 2015, is available online via doi: 10.1093/mnras/stv2571 Published by Oxford University Press on behalf of the Royal Astronomical Society. Copyright 2015 The AuthorsRadio emission from radio-quiet quasars may be due to star formation in the quasar host galaxy, to a jet launched by the supermassive black hole, or to relativistic particles accelerated in a wide-angle radiatively driven outflow. In this paper, we examine whether radio emission from radio-quiet quasars is a byproduct of star formation in their hosts. To this end, we use infrared spectroscopy and photometry from Spitzer and Herschel to estimate or place upper limits on star formation rates in hosts of ∼300 obscured and unobscured quasars at z < 1. We find that low-ionization forbidden emission lines such as [Ne II] and [Ne III] are likely dominated by quasar ionization and do not provide reliable star formation diagnostics in quasar hosts, while polycyclic aromatic hydrocarbon (PAH) emission features may be suppressed due to the destruction of PAH molecules by the quasar radiation field. While the bolometric luminosities of our sources are dominated by the quasars, the 160 μm fluxes are likely dominated by star formation, but they too should be used with caution. We estimate median star formation rates to be 6–29 M yr−1, with obscured quasars at the high end of this range. This star formation rate is insufficient to explain the observed radio emission from quasars by an order of magnitude, with log (Lradio, obs/Lradio, SF) = 0.6–1.3 depending on quasar type and star formation estimator. Although radio-quiet quasars in our sample lie close to the 8–1000 μm infrared/radio correlation characteristic of the star-forming galaxies, both their infrared emission and their radio emission are dominated by the quasar activity, not by the host galaxy.Peer reviewedFinal Published versio

A Brain Region-Specific Predictive Gene Map for Autism Derived by Profiling a Reference Gene Set

Molecular underpinnings of complex psychiatric disorders such as autism spectrum disorders (ASD) remain largely unresolved. Increasingly, structural variations in discrete chromosomal loci are implicated in ASD, expanding the search space for its disease etiology. We exploited the high genetic heterogeneity of ASD to derive a predictive map of candidate genes by an integrated bioinformatics approach. Using a reference set of 84 Rare and Syndromic candidate ASD genes (AutRef84), we built a composite reference profile based on both functional and expression analyses. First, we created a functional profile of AutRef84 by performing Gene Ontology (GO) enrichment analysis which encompassed three main areas: 1) neurogenesis/projection, 2) cell adhesion, and 3) ion channel activity. Second, we constructed an expression profile of AutRef84 by conducting DAVID analysis which found enrichment in brain regions critical for sensory information processing (olfactory bulb, occipital lobe), executive function (prefrontal cortex), and hormone secretion (pituitary). Disease specificity of this dual AutRef84 profile was demonstrated by comparative analysis with control, diabetes, and non-specific gene sets. We then screened the human genome with the dual AutRef84 profile to derive a set of 460 potential ASD candidate genes. Importantly, the power of our predictive gene map was demonstrated by capturing 18 existing ASD-associated genes which were not part of the AutRef84 input dataset. The remaining 442 genes are entirely novel putative ASD risk genes. Together, we used a composite ASD reference profile to generate a predictive map of novel ASD candidate genes which should be prioritized for future research

Natural malaria infection elicits rare but potent neutralizing antibodies to the blood-stage antigen RH5

Plasmodium falciparum reticulocyte-binding protein homolog 5 (RH5) is the most advanced blood-stage malaria vaccine candidate and is being evaluated for efficacy in endemic regions, emphasizing the need to study the underlying antibody response to RH5 during natural infection, which could augment or counteract responses to vaccination. Here, we found that RH5-reactive B cells were rare, and circulating immunoglobulin G (IgG) responses to RH5 were short-lived in malaria-exposed Malian individuals, despite repeated infections over multiple years. RH5-specific monoclonal antibodies isolated from eight malaria-exposed individuals mostly targeted non-neutralizing epitopes, in contrast to antibodies isolated from five RH5-vaccinated, malaria-naive UK individuals. However, MAD8-151 and MAD8-502, isolated from two malaria-exposed Malian individuals, were among the most potent neutralizers out of 186 antibodies from both cohorts and targeted the same epitopes as the most potent vaccine-induced antibodies. These results suggest that natural malaria infection may boost RH5-vaccine-induced responses and provide a clear strategy for the development of next-generation RH5 vaccines

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead