223 research outputs found

    SNLS3: Constraints on Dark Energy Combining the Supernova Legacy Survey Three Year Data with Other Probes

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    We present observational constraints on the nature of dark energy using the Supernova Legacy Survey three year sample (SNLS3) of Guy et al. (2010) and Conley et al. (2011). We use the 472 SNe Ia in this sample, accounting for recently discovered correlations between SN Ia luminosity and host galaxy properties, and include the effects of all identified systematic uncertainties directly in the cosmological fits. Combining the SNLS3 data with the full WMAP7 power spectrum, the Sloan Digital Sky Survey luminous red galaxy power spectrum, and a prior on the Hubble constant H0 from SHOES, in a flat universe we find omega_m=0.269+/-0.015 and w=-1.061+0.069-0.068 -- a 6.5% measure of the dark energy equation-of-state parameter w. The statistical and systematic uncertainties are approximately equal, with the systematic uncertainties dominated by the photometric calibration of the SN Ia fluxes -- without these calibration effects, systematics contribute only a ~2% error in w. When relaxing the assumption of flatness, we find omega_m=0.271+/-0.015, omega_k=-0.002+/-0.006, and w=-1.069+0.091-0.092. Parameterizing the time evolution of w as w(a)=w_0+w_a(1-a), gives w_0=-0.905+/-0.196, w_a=-0.984+1.094-1.097 in a flat universe. All of our results are consistent with a flat, w=-1 universe. The size of the SNLS3 sample allows various tests to be performed with the SNe segregated according to their light curve and host galaxy properties. We find that the cosmological constraints derived from these different sub-samples are consistent. There is evidence that the coefficient, beta, relating SN Ia luminosity and color, varies with host parameters at >4sigma significance (in addition to the known SN luminosity--host relation); however this has only a small effect on the cosmological results and is currently a sub-dominant systematic.Comment: Accepted for publication in ApJ. Data available from https://tspace.library.utoronto.ca/snl

    Type Ia Supernova host galaxies as seen with IFU spectroscopy

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    (abridged) We used the wide-field IFU spectrograph PMAS/PPAK at the 3.5m telescope of Calar Alto Observatory to observe six nearby spiral galaxies that hosted SNe Ia. Spatially resolved 2D maps of the properties of the ionized gas and the stellar populations were derived. Five of the observed galaxies have an ongoing star formation rate of 1-5 M_sun/yr and mean stellar population ages ~5 Gyr. The sixth galaxy shows no star formation and has an about 12 Gyr old stellar population. All galaxies have stellar masses larger than 2E+10 M_sun and metallicities above solar. Four galaxies show negative radial metallicity gradients of the ionized gas up to -0.058 dex/kpc and one has nearly uniform metallicity with a possible shallow positive slope. The stellar components show shallower negative metallicity gradients up to -0.03 dex/kpc. We find no clear correlation between the properties of the galaxy and those of the supernovae, which may be because of the small ranges spanned by the galaxy parameters. However, we note that the Hubble residuals are on average positive while negative Hubble residuals are expected for SNe Ia in massive hosts such as the galaxies in our sample. In conclusion, IFU spectroscopy on 4-m telescopes is a viable technique for studying host galaxies of nearby SNe Ia. It allows one to correlate the supernova properties with the properties of their host galaxies at the projected positions of the supernovae. Our current sample of six galaxies is too small to draw conclusions about the SN Ia progenitors or correlations with the galaxy properties, but the ongoing CALIFA IFU survey will provide a solid basis to exploit this technique more and improve our understanding of SNe Ia as cosmological standard candles.Comment: accepted by A&A, final language-edited version, layout change

    Eating disorders: from twin studies to candidate genes and beyond

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    Substantial effort has been put into the exploration of the biological background of eating disorders, through family, twin and molecular genetic studies. Family studies have shown that anorexia (AN) and bulimia nervosa (BN) are strongly familial, and that familial etiologic factors appear to be shared by both disorders. Twin studies often focus on broader phenotypes or subthreshold eating disorders. These studies consistently yielded moderate to substantial heritabilities. In addition, there has been a proliferation of molecular genetic studies that focused on Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) AN and BN. Seven linkage regions have been identified in genome-wide screens. Many genetic association studies have been performed, but no consistent association between a candidate gene and AN or BN has been reported. Larger genetic association studies and collaborations are needed to examine the involvement of several candidate genes and biological pathways in eating disorders. In addition, twin studies should be designed to assist the molecular work by further exploring genetic determinants of endophenotypes, evaluating the magnitude of contribution to liability of measured genotypes as well as environmental risk factors related to eating disorders. In this manner twin and molecular studies can move the field forward in a mutually informative way

    SMC complexes differentially compact mitotic chromosomes according to genomic context

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    Structural maintenance of chromosomes (SMC) protein complexes are key determinants of chromosome conformation. Using Hi-C and polymer modelling, we study how cohesin and condensin, two deeply conserved SMC complexes, organize chromosomes in the budding yeast Saccharomyces cerevisiae. The canonical role of cohesin is to co-align sister chromatids, while condensin generally compacts mitotic chromosomes. We find strikingly different roles for the two complexes in budding yeast mitosis. First, cohesin is responsible for compacting mitotic chromosome arms, independently of sister chromatid cohesion. Polymer simulations demonstrate that this role can be fully accounted for through cis-looping of chromatin. Second, condensin is generally dispensable for compaction along chromosome arms. Instead, it plays a targeted role compacting the rDNA proximal regions and promoting resolution of peri-centromeric regions. Our results argue that the conserved mechanism of SMC complexes is to form chromatin loops and that distinct SMC-dependent looping activities are selectively deployed to appropriately compact chromosomes

    Staphylococcal Enterotoxins

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    Staphylococcus aureus (S. aureus) is a Gram positive bacterium that is carried by about one third of the general population and is responsible for common and serious diseases. These diseases include food poisoning and toxic shock syndrome, which are caused by exotoxins produced by S. aureus. Of the more than 20 Staphylococcal enterotoxins, SEA and SEB are the best characterized and are also regarded as superantigens because of their ability to bind to class II MHC molecules on antigen presenting cells and stimulate large populations of T cells that share variable regions on the Ξ² chain of the T cell receptor. The result of this massive T cell activation is a cytokine bolus leading to an acute toxic shock. These proteins are highly resistant to denaturation, which allows them to remain intact in contaminated food and trigger disease outbreaks. A recognized problem is the emergence of multi-drug resistant strains of S. aureus and these are a concern in the clinical setting as they are a common cause of antibiotic-associated diarrhea in hospitalized patients. In this review, we provide an overview of the current understanding of these proteins

    Recent research on Gulf War illness and other health problems in veterans of the 1991 Gulf War: Effects of toxicant exposures during deployment

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    Veterans of Operation Desert Storm/Desert Shield - the 1991 Gulf War (GW) - are a unique population who returned from theater with multiple health complaints and disorders. Studies in the U.S. and elsewhere have consistently concluded that approximately 25-32% of this population suffers from a disorder characterized by symptoms that vary somewhat among individuals and include fatigue, headaches, cognitive dysfunction, musculoskeletal pain, and respiratory, gastrointestinal and dermatologic complaints. Gulf War illness (GWI) is the term used to describe this disorder. In addition, brain cancer occurs at increased rates in subgroups of GW veterans, as do neuropsychological and brain imaging abnormalities. Chemical exposures have become the focus of etiologic GWI research because nervous system symptoms are prominent and many neurotoxicants were present in theater, including organophosphates (OPs), carbamates, and other pesticides; sarin/cyclosarin nerve agents, and pyridostigmine bromide (PB) medications used as prophylaxis against chemical warfare attacks. Psychiatric etiologies have been ruled out. This paper reviews the recent literature on the health of 1991 GW veterans, focusing particularly on the central nervous system and on effects of toxicant exposures. In addition, it emphasizes research published since 2008, following on an exhaustive review that was published in that year that summarizes the prior literature (RACGWI, 2008). We conclude that exposure to pesticides and/or to PB are causally associated with GWI and the neurological dysfunction in GW veterans. Exposure to sarin and cyclosarin and to oil well fire emissions are also associated with neurologically based health effects, though their contribution to development of the disorder known as GWI is less clear. Gene-environment interactions are likely to have contributed to development of GWI in deployed veterans. The health consequences of chemical exposures in the GW and other conflicts have been called "toxic wounds" by veterans. This type of injury requires further study and concentrated treatment research efforts that may also benefit other occupational groups with similar exposure-related illnesses
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