143 research outputs found

    Taxonomic validity of Mesoclemmys heliostemma (McCord, Joseph-Ouni & Lamar, 2001) (Testudines, Chelidae) inferred from morphological analysis

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    Mesoclemmys heliostemma (Testudines: Chelidae) was described based on five vouchered specimens and nine live specimens from the western Amazon basin. Some authors questioned its status as a valid species, suggesting that it represents a junior synonym of M. raniceps. Here, we report on eight additional specimens from eastern Peru and northern Brazil, and provide descriptive statistics of morphological characters for hatchlings, juveniles, and adults of M. heliostemma, M. raniceps, and M. gibba. We also test for group differences through univariate and multivariate statistical analyses, and discuss some advantages of this methodology. Our data suggest that all three taxa are morphologically divergent, and that M. heliostemma is a valid species.Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (BIOTA/FAPESP) [02/13602-4, 11/50206-9]Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (BIOTA/FAPESP)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [565046/2010-1, 303545/2010-0

    Observation of J/ψpJ/\psi p resonances consistent with pentaquark states in Λb0J/ψKp{\Lambda_b^0\to J/\psi K^-p} decays

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    Observations of exotic structures in the J/ψpJ/\psi p channel, that we refer to as pentaquark-charmonium states, in Λb0J/ψKp\Lambda_b^0\to J/\psi K^- p decays are presented. The data sample corresponds to an integrated luminosity of 3/fb acquired with the LHCb detector from 7 and 8 TeV pp collisions. An amplitude analysis is performed on the three-body final-state that reproduces the two-body mass and angular distributions. To obtain a satisfactory fit of the structures seen in the J/ψpJ/\psi p mass spectrum, it is necessary to include two Breit-Wigner amplitudes that each describe a resonant state. The significance of each of these resonances is more than 9 standard deviations. One has a mass of 4380±8±294380\pm 8\pm 29 MeV and a width of 205±18±86205\pm 18\pm 86 MeV, while the second is narrower, with a mass of 4449.8±1.7±2.54449.8\pm 1.7\pm 2.5 MeV and a width of 39±5±1939\pm 5\pm 19 MeV. The preferred JPJ^P assignments are of opposite parity, with one state having spin 3/2 and the other 5/2.Comment: 48 pages, 18 figures including the supplementary material, v2 after referee's comments, now 19 figure

    Blood Meal-Derived Heme Decreases ROS Levels in the Midgut of Aedes aegypti and Allows Proliferation of Intestinal Microbiota

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    The presence of bacteria in the midgut of mosquitoes antagonizes infectious agents, such as Dengue and Plasmodium, acting as a negative factor in the vectorial competence of the mosquito. Therefore, knowledge of the molecular mechanisms involved in the control of midgut microbiota could help in the development of new tools to reduce transmission. We hypothesized that toxic reactive oxygen species (ROS) generated by epithelial cells control bacterial growth in the midgut of Aedes aegypti, the vector of Yellow fever and Dengue viruses. We show that ROS are continuously present in the midgut of sugar-fed (SF) mosquitoes and a blood-meal immediately decreased ROS through a mechanism involving heme-mediated activation of PKC. This event occurred in parallel with an expansion of gut bacteria. Treatment of sugar-fed mosquitoes with increased concentrations of heme led to a dose dependent decrease in ROS levels and a consequent increase in midgut endogenous bacteria. In addition, gene silencing of dual oxidase (Duox) reduced ROS levels and also increased gut flora. Using a model of bacterial oral infection in the gut, we show that the absence of ROS resulted in decreased mosquito resistance to infection, increased midgut epithelial damage, transcriptional modulation of immune-related genes and mortality. As heme is a pro-oxidant molecule released in large amounts upon hemoglobin degradation, oxidative killing of bacteria in the gut would represent a burden to the insect, thereby creating an extra oxidative challenge to the mosquito. We propose that a controlled decrease in ROS levels in the midgut of Aedes aegypti is an adaptation to compensate for the ingestion of heme

    Measurement of the Ξ<sup>-</sup><sub>b</sub> and Ω<sup>-</sup><sub>b</sub> baryon lifetimes

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    Using a data sample of pp collisions corresponding to an integrated luminosity of 3 fb13~ \rm fb^{-1}, the Ξb\Xi_b^- and Ωb\Omega_b^- baryons are reconstructed in the ΞbJ/ψΞ\Xi_b^- \rightarrow J/\psi \Xi^- and ΩbJ/ψΩ\Omega_b^- \rightarrow J/\psi \Omega^- decay modes and their lifetimes measured to be \tau (\Xi_b^-) = 1.55\, ^{+0.10}_{-0.09}~{\rm(stat)} \pm 0.03\,{\rm(syst)} ps, \tau (\Omega_b^-) = 1.54\, ^{+0.26}_{-0.21}~{\rm(stat)} \pm 0.05\,{\rm(syst)} ps. These are the most precise determinations to date. Both measurements are in good agreement with previous experimental results and with theoretical predictions

    First observation and amplitude analysis of the B−→D+K−π− decay

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    The B−→D+K−π− decay is observed in a data sample corresponding to 3.0  fb−1 of pp collision data recorded by the LHCb experiment during 2011 and 2012. Its branching fraction is measured to be B(B−→D+K−π−)=(7.31±0.19±0.22±0.39)×10−5 where the uncertainties are statistical, systematic and from the branching fraction of the normalization channel B−→D+π−π−, respectively. An amplitude analysis of the resonant structure of the B−→D+K−π− decay is used to measure the contributions from quasi-two-body B−→D∗0(2400)0K−, B−→D∗2(2460)0K−, and B−→D∗J(2760)0K− decays, as well as from nonresonant sources. The D∗J(2760)0 resonance is determined to have spin 1

    Novel Common Genetic Susceptibility Loci for Colorectal Cancer

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    BACKGROUND: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk. METHODS: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided. RESULTS: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0. CONCLUSIONS: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screenin
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