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

Stribild: A Review of Component Characteristics and Combination Drug Efficacy

BACKGROUND: Numerous methods have been devised to combat human immunodeficiency virus (HIV) replication and disease progression. Composed of an integrase strand transfer inhibitor, a pharmacoenhancer, and two reverse transcriptase inhibitors, Stribild is a relatively new combination HIV drug formulated for once-a-day dosing. METHODS: Relevant information, original research articles and reviews, were gathered primarily through the use of the PubMed database. The search was conducted without date restrictions in order to collect both historical and recent information concerning HIV, individual drugs, and combinations for a thorough overview. RESULTS: Stribild, when taken with food, provides therapeutic drug concentrations as seen through comparison with the respective individual or boosted individual drugs. Stribild non-inferiority has been shown when compared to other HIV drug combinations, ritonavir-boosted atazanavir or efavirenz each with a tenofovir disoproxil fumarate (TDF) and emtricitabine (FTC) backbone. The co-formulation also retained high viral suppression in patients switching from other regimens, such as efavirenz/TDF/FTC, raltegravir/TDF/FTC, or various ritonavir-boosted protease inhibitors with TDF/FTC. The elvitegravir and cobicistat combination was unaffected by moderate hepatic impairment; however, hepatic and renal function along with changes in bone mineral density should be monitored closely. Stribild presented with relatively few side effect occurrences, but drug interactions may pose a larger problem for continuous therapy. CONCLUSIONS: Stribild provides viral suppression, comparable to other combination HIV drugs through review of non-inferiority and regimen simplification studies, with minimal adverse effects. Although the breadth of Stribild effectiveness has begun to unfold, studies are lacking in older patients as well as adolescents

Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapyinduced leukemia

Glutathione S-transferases (GSTs) detoxify potentially mutagenic and toxic DNA-reactive electrophiles, including metabolites of several chemotherapeutic agents, some of which are suspected human carcinogens. Functional polymorphisms exist in at least three genes that encode GSTs, including GSTM1, GSTT1, and GSTP1. We hypothesize, therefore, that polymorphisms in genes that encode GSTs alter susceptibility to chemotherapy-induced carcinogenesis, specifically to therapy-related acute myeloid leukemia (t-AML), a devastating complication of long-term cancer survival. Elucidation of genetic determinants may help to identify individuals at increased risk of developing t-AML. To this end, we have examined 89 cases of t-AML, 420 cases of de novo AML, and 1,022 controls for polymorphisms in GSTM1, GSTT1, and GSTP1. Gene deletion of GSTM1 or GSTT1 was not specifically associated with susceptibility to t-AML. Individuals with at least one GSTP1 codon 105 Val allele were significantly over-represented in t-AML cases compared with de novo AML cases [odds ratio (OR), 1.81; 95% confidence interval (CI), 1.11–2.94]. Moreover, relative to de novo AML, the GSTP1 codon 105 Val allele occurred more often among t-AML patients with prior exposure to chemotherapy (OR, 2.66; 95% CI, 1.39–5.09), particularly among those with prior exposure to known GSTP1 substrates (OR, 4.34; 95% CI, 1.43–13.20), and not among those t-AML patients with prior exposure to radiotherapy alone (OR,1.01; 95% CI, 0.50–2.07). These data suggest that inheritance of at least one Val allele at GSTP1 codon 105 confers a significantly increased risk of developing t-AML after cytotoxic chemotherapy, but not after radiotherapy

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