The HI Mass Function and Velocity Width Function of Void Galaxies in the Arecibo Legacy Fast ALFA Survey

We measure the HI mass function (HIMF) and velocity width function (WF) across environments over a range of masses $7.2<\log(M_{HI}/M_{\odot})<10.8$, and profile widths $1.3\log(km/s)<\log(W)<2.9\log(km/s)$, using a catalog of ~7,300 HI-selected galaxies from the ALFALFA Survey, located in the region of sky where ALFALFA and SDSS (Data Release 7) North overlap. We divide our galaxy sample into those that reside in large-scale voids (void galaxies) and those that live in denser regions (wall galaxies). We find the void HIMF to be well fit by a Schechter function with normalization $\Phi^*=(1.37\pm0.1)\times10^{-2} h^3Mpc^{-3}$, characteristic mass $\log(M^*/M_{\odot})+2\log h_{70}=9.86\pm0.02$, and low-mass-end slope $\alpha=-1.29\pm0.02$. Similarly, for wall galaxies, we find best-fitting parameters $\Phi^*=(1.82\pm0.03)\times10^{-2} h^3Mpc^{-3}$, $\log(M^*/M_{\odot})+2\log h_{70}=10.00\pm0.01$, and $\alpha=-1.35\pm0.01$. We conclude that void galaxies typically have slightly lower HI masses than their non-void counterparts, which is in agreement with the dark matter halo mass function shift in voids assuming a simple relationship between DM mass and HI mass. We also find that the low-mass slope of the void HIMF is similar to that of the wall HIMF suggesting that there is either no excess of low-mass galaxies in voids or there is an abundance of intermediate HI mass galaxies. We fit a modified Schechter function to the ALFALFA void WF and determine its best-fitting parameters to be $\Phi^*=0.21\pm0.1 h^3Mpc^{-3}$, $\log(W^*)=2.13\pm0.3$, $\alpha=0.52\pm0.5$ and high-width slope $\beta=1.3\pm0.4$. For wall galaxies, the WF parameters are: $\Phi^*=0.022\pm0.009 h^3Mpc^{-3}$, $\log(W^*)=2.62\pm0.5$, $\alpha=-0.64\pm0.2$ and $\beta=3.58\pm1.5$. Because of large uncertainties on the void and wall width functions, we cannot conclude whether the WF is dependent on the environment.Comment: Accepted for publication at MNRAS, 14 pages, 12 figure

Mutations in the E2 glycoprotein and the 3\u27 untranslated region enhance chikungunya virus virulence in mice

Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus that causes debilitating musculoskeletal pain and inflammation and can persist for months to years after acute infection. Although studies of humans and experimentally infected animals suggest that CHIKV infection persists in musculoskeletal tissues, the mechanisms for this remain poorly understood. To evaluate this further, we isolated CHIKV from the serum of persistently infected Rag1 -/- mice at day 28. When inoculated into naive wild-type (WT) mice, this persistently circulating CHIKV strain displayed a capacity for earlier dissemination and greater pathogenicity than the parental virus. Sequence analysis revealed a nonsynonymous mutation in the E2 glycoprotein (E2 K200R) and a deletion within the 3' untranslated region (3'-UTR). The introduction of these changes into the parental virus conferred enhanced virulence in mice, although primary tropism for musculoskeletal tissues was maintained. The E2 K200R mutation was largely responsible for enhanced viral dissemination and pathogenicity, although these effects were augmented by the 3'- UTR deletion. Finally, studies with Irf3/Irf7 -/- and Ifnar1 -/- mice suggest that the E2 K200R mutation enhances viral dissemination from the site of inoculation independently of interferon regulatory factor 3 (IRF3)-, IRF7-, and IFNAR1-mediated responses. As our findings reveal viral determinants of CHIKV dissemination and pathogenicity, their further study should help to elucidate host-virus interactions that determine acute and chronic CHIKV infection

Survey of Canada Goose Feces for Presence of \u3cem\u3eGiardia\u3c/em\u3e

As resident Canada goose (Branta canadensis) populations increase throughout North America, so do the health and environmental risks associated with goose feces. Previous studies suggest that goose feces may be a conduit for transmitting Giardia, a protozoan that is parasitic to humans. We surveyed fecal droppings from free-ranging resident Canada geese for Giardia spp. at 9 sites in the Triangle area (Raleigh, Durham, and Chapel Hill) of North Carolina in 2007 and 2008. Samples (n = 234) were tested using the ProSpect® Giardia EZ Microplate Assay, and there were no positives. Our results indicate that risk of zoonotic giardiasis from Canada goose feces in the Triangle area of North Carolina is low

Manganese superoxide dismutase Ala-9Val polymorphism and risk of breast cancer in a population-based case–control study of African Americans and whites

INTRODUCTION: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies. Results suggest that the Ala allele increases the risk of breast cancer and modifies the effects of environmental exposures that produce oxidative damage to DNA. METHODS: We examined the role of the MnSOD Ala-9Val polymorphism in a population-based case–control study of invasive and in situ breast cancer in North Carolina. Genotypes were evaluated for 2025 cases (760 African Americans and 1265 whites) and for 1812 controls (677 African Americans and 1135 whites). RESULTS: The odds ratio for MnSOD Ala/Ala versus any MnSOD Val genotypes was not elevated in African Americans (odds ratio = 0.9, 95% confidence interval = 0.7–1.2) or in whites (odds ratio = 1.0, 95% confidence interval = 0.8–1.2). Greater than additive joint effects were observed for the Ala/Ala genotype and smoking, radiation to the chest, and occupational exposure to ionizing radiation. Antagonism was observed between the Ala/Ala genotype and the use of nonsteroidal anti-inflammatory drugs. CONCLUSIONS: The MnSOD genotype may contribute to an increased risk of breast cancer in the presence of specific environmental exposures. These results provide further evidence for the importance of reactive oxygen species and of oxidative DNA damage in the etiology of breast cancer