482 research outputs found

    Some Results for the Chromatic Correction of the Antisymmetric RHIC Lattice

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    Coarse-grained simulations of material shock compression: interplay between mechanics, thermals, and chemistry

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    We present a coarse-graining model that enables the description of pressure-induced, endothermic reactions in a model material. An additional implicit variable (the particle size) is used to describe particles undergoing volume-reducing endothermic reactions via a bistable intra-molecular potential, whereas the dynamics of the center-of-mass motion evolves according to interparticle forces. The equations of motion are derived from a Hamiltonian and the model exhibits two desired features: total energy conservation and Galilean invariance. In this study, we explore a simple model material with pairwise interactions between particles to study pressure-induced chemical reactions under both quasi-static and shock loading conditions. Our results demonstrate that such model can capture the complex mechanical processes arising from the interplay between deformation defects and chemical reactions. Moreover, we explore the feasibility to realize a material with such characteristics that can be used to attenuate the energy in sustained shocks which is of interest in many applications

    A Chromatic Correction Scheme for the RHIC3 Lattice

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    This report is about the Chromatic Correction Scheme for the RHIC3 Lattice. The RHIC3 is the current design for the relativistic heavy ion collider

    Preliminary Chromatic Correction

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    A Chromatic Correction Scheme for the Antisymmetric RHIC Lattice. The First Approximation

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    This report describes the Chromatic Correction Scheme for the Antisymmetric RHIC Lattice. The First Approximation

    Insights from quantitative and mathematical modelling on the proposed 2030 goal for gambiense human African trypanosomiasis (gHAT)

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    Gambiense human African trypanosomiasis (gHAT) is a parasitic, vector-borne neglected tropical disease that has historically affected populations across West and Central Africa and can result in death if untreated. Following from the success of recent intervention programmes against gHAT, the World Health Organization (WHO) has defined a 2030 goal of global elimination of transmission (EOT). The key proposed indicator to measure achievement of the goal is to have zero reported cases. Results of previous mathematical modelling and quantitative analyses are brought together to explore both the implications of the proposed indicator and the feasibility of achieving the WHO goal. Whilst the indicator of zero case reporting is clear and measurable, it is an imperfect proxy for EOT and could arise either before or after EOT is achieved. Lagging reporting of infection and imperfect diagnostic specificity could result in case reporting after EOT, whereas the converse could be true due to underreporting, lack of coverage, and cryptic human and animal reservoirs. At the village-scale, the WHO recommendation of continuing active screening until there are three years of zero cases yields a high probability of local EOT, but extrapolating this result to larger spatial scales is complex. Predictive modelling of gHAT has consistently found that EOT by 2030 is unlikely across key endemic regions if current medical-only strategies are not bolstered by improved coverage, reduced time to detection and/or complementary vector control. Unfortunately, projected costs for strategies expected to meet EOT are high in the short term and strategies that are cost-effective in reducing burden are unlikely to result in EOT by 2030. Future modelling work should aim to provide predictions while taking into account uncertainties in stochastic dynamics and infection reservoirs, as well as assessment of multiple spatial scales, reactive strategies, and measurable proxies of EOT

    Mutational Activation of ras Genes is Absent in Pediatric Osteosarcoma

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    Activation of ras oncogenes is found in human cancers; overall it is observed in 15% of all neoplasms. The purpose of this study was to assess the extent of involvement of ras oncogenes in osteosarcoma. Tumor samples from a series of 49 pediatric patients diagnosed with osteosarcoma and treated at our institution were evaluated. Paraffin-embedded tumor samples from diagnostic biopsies, from tumor en bloc resection tissue after neoadjuvant chemotherapy, and samples from metastases were examined in search of point mutations in H, K, and N-ras genes at codons 12 and 61 by means of polymerase chain reaction (PCR), slot-blotting, and radioactive labeled specific DNA probes. A total of 92 archival samples were studied. No point mutations activating these genes were found. These findings suggest that the activation by point mutations at codons 12 and 61 of the H, K, and N-ras genes does not play a role in the pathogenesis of human osteosarcoma. Since no point mutations in codons 12 and 61 were detected, it was not possible to establish any correlation between the ras genes and clinical or histologic finding
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