The impact of small-scale turbulence on laminar magnetic reconnection

Initial states in incompressible two-dimensional magnetohydrodynamics that are known to lead to strong current sheets and (laminar) magnetic reconnection are modified by the addition of small-scale turbulent perturbations of various energies. The evolution of these states is computed with the aim of ascertaining the influence of the turbulence on the underlying laminar solution. Two main questions are addressed here: (1) What effect does small-scale turbulence have on the energy dissipation rate of the underlying solution? (2) What is the threshold turbulent perturbation level above which the original laminar reconnective dynamics is no longer recognizable. The simulations show that while the laminar dynamics persist the dissipation rates are largely unaffected by the turbulence, other than modest increases attributable to the additional small length scales present in the new initial condition. The solutions themselves are also remarkably insensitive to small-scale turbulent perturbations unless the perturbations are large enough to undermine the integrity of the underlying cellular flow pattern. Indeed, even initial states that lead to the evolution of small-scale microscopic sheets can survive the addition of modest turbulence. The role of a large-scale organizing background magnetic field is also addressed

Elucidating the Mechanism of Action of Experimental Compound SW33 in Toxoplasma gondii

In recent years, antimicrobial drug resistance has become widespread and thus triggered an ever-growing need for the development of new, efficacious drug treatments. As an antimicrobial drug is developed, its mechanism of action is often identified before it becomes a potential candidate for clinical use. One potential method for identifying mechanism of action is chemical mutagenesis, in which induction of drug-resistant populations is followed by whole-genome sequencing of several clonal isolates. The subsequent observation of identical point mutations in the same gene across multiple drug-resistant populations can indicate a likely molecular target. However, this technique lacks the capacity to facilitate speedy and robust elucidation of the mechanism of action of experimental compounds, indicating a need for improved methods to enhance the efficiency of high-throughput drug target identification. In this work, a novel technique utilizing double chemical mutagenesis was developed in order to quickly induce the high levels of resistance indicative of specific resistance in the apicomplexan parasiteToxoplasma gondii. This technique is being used to identify drug targets in experimental compound, SW33, that has shown efficacy against T. gondii