2,121 research outputs found
Truncated Product Representations for L-Functions in the Hyperelliptic Ensemble
This is the author accepted manuscript. The final version is available from the publisher via the DOI in this recordWe investigate the approximation of quadratic Dirichlet L-functions over function fields by truncations of their Euler products. We first establish representations for such L-functions as products over prime polynomials times products over their zeros. This is the hybrid formula in function fields. We then prove that partial Euler products are good approximations of an L-function away from its zeros, and that, when the length of the product tends to infinity, we recover the original L-function. We also obtain explicit expressions for the arguments of quadratic Dirichlet L-functions over function fields and for the arguments of their partial Euler products. In the second part of the paper we construct, for each quadratic Dirichlet L-function over a function field, an auxiliary function based on the approximate functional equation that equals the L-function on the critical line. We also construct a parametrized family of approximations of these auxiliary functions, prove the Riemann hypothesis holds for them, and that their zeros are related to those of the associated L-function. Finally, we estimate the counting function for the zeros of this family of approximations, show that these zeros cluster near those of the associated L-function, and that, when the parameter is not too large, almost all the zeros of the approximations are simple.JCA was partially supported by a Research in Pairs - Scheme 4 London Mathematical Society grant. SMG was supported in part by National Science Foundation Grant DMS-1200582. JPK gratefully acknowledges support under EPSRC Programme Grant EP/K034383/1 (LMF: L-Functions and Modular Forms) and a Royal Society Wolfson Research Merit Award
Data on mortality from external causes and events of undetermined intent, Parana State, Brazil, 1979 to 2005
This study analyzed the quality of data from the Mortality Information System (SIM) for deaths due to external causes in the State of Parana, Brazil, 1979 to 2005, focusing on events of undetermined intent. Deaths were grouped in motor vehicle accidents, homicides, suicides, and events of undetermined intent, and proportional mortality and relative annual variation of rates over the three-year period were analyzed. Motor vehicle accidents (more than 30% of the total) were the most frequent causes of death throughout the period, and since 1997 homicides have become the second most frequent cause. Deaths due to events of undetermined intent caused by weapons (firearms or knives) decreased from 4.8% in 1981 to 0.3% in 2005. Mortality rates for events of undetermined intent (overall) decreased from 14.9 deaths per 100,000 inhabitants in 1979-81 to 2.0 in 2003-05. Annual percentage variation was 13.1% from 1980 to 1985, -6% from 1996 to 2000, and -11% from 2000 to 2004. The findings show the good quality of SIM data on external causes in the State of Parana, allowing analyses with the potential to support programs to prevent injuries as well as health promotion measures.25122322
Benznidazole biotransformation and multiple targets in <i>Trypanosoma</i> cruzi revealed by metabolomics
<b>Background</b><p></p>
The first line treatment for Chagas disease, a neglected tropical disease caused by the protozoan parasite Trypanosoma cruzi, involves administration of benznidazole (Bzn). Bzn is a 2-nitroimidazole pro-drug which requires nitroreduction to become active, although its mode of action is not fully understood. In the present work we used a non-targeted MS-based metabolomics approach to study the metabolic response of T. cruzi to Bzn.<p></p>
<b>Methodology/Principal findings</b><p></p>
Parasites treated with Bzn were minimally altered compared to untreated trypanosomes, although the redox active thiols trypanothione, homotrypanothione and cysteine were significantly diminished in abundance post-treatment. In addition, multiple Bzn-derived metabolites were detected after treatment. These metabolites included reduction products, fragments and covalent adducts of reduced Bzn linked to each of the major low molecular weight thiols: trypanothione, glutathione, γ-glutamylcysteine, glutathionylspermidine, cysteine and ovothiol A. Bzn products known to be generated in vitro by the unusual trypanosomal nitroreductase, TcNTRI, were found within the parasites, but low molecular weight adducts of glyoxal, a proposed toxic end-product of NTRI Bzn metabolism, were not detected.<p></p>
<b>Conclusions/significance</b><p></p>
Our data is indicative of a major role of the thiol binding capacity of Bzn reduction products in the mechanism of Bzn toxicity against T. cruzi
Perspectives on the Trypanosoma cruzi-host cell receptor interaction
Chagas disease is caused by the parasite Trypanosoma cruzi. The critical initial event is the interaction of the trypomastigote form of the parasite with host receptors. This review highlights recent observations concerning these interactions. Some of the key receptors considered are those for thromboxane, bradykinin, and for the nerve growth factor TrKA. Other important receptors such as galectin-3, thrombospondin, and laminin are also discussed. Investigation into the molecular biology and cell biology of host receptors for T. cruzi may provide novel therapeutic targets
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