936 research outputs found

    Assessment of progress towards the eradication of dracunculiasis in the Afram Plains, Ghana

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    Infectious mononucleosis

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    This issue of eMedRef provides information to clinicians on the pathophysiology, diagnosis, and therapeutics of infectious mononucleosis

    Enabling Real-Time Ultrasound Imaging of Soft Tissue Mechanical Properties by Simplification of the Shear Wave Motion Equation

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    Ultrasound based shear wave elastography (SWE) is a technique used for non-invasive characterization and imaging of soft tissue mechanical properties. Robust estimation of shear wave propagation speed is essential for imaging of soft tissue mechanical properties. In this study we propose to estimate shear wave speed by inversion of the firstorder wave equation following directional filtering. This approach relies on estimation of first-order derivatives which allows for accurate estimations using smaller smoothing filters than when estimating second-order derivatives. The performance was compared to three current methods used to estimate shear wave propagation speed: direct inversion of the wave equation (DIWE), time-to-peak (TTP) and crosscorrelation (CC). The shear wave speed of three homogeneous phantoms of different elastic moduli (gelatin by weight of 5%, 7%, and 9%) were measured with each method. The proposed method was shown to produce shear speed estimates comparable to the conventional methods (standard deviation of measurements being 0.13 m/s, 0.05 m/s, and 0.12 m/s), but with simpler processing and usually less time (by a factor of 1, 13, and 20 for DIWE, CC, and TTP respectively). The proposed method was able to produce a 2-D speed estimate from a single direction of wave propagation in about four seconds using an off-the-shelf PC, showing the feasibility of performing real-time or near real-time elasticity imaging with dedicated hardware

    Accessing dark states optically through excitation-ferrying states

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    The efficiency of solar energy harvesting systems is largely determined by their ability to transfer excitations from the antenna to the energy trapping center before recombination. Dark state protection, achieved by coherent coupling between subunits in the antenna structure, can significantly reduce radiative recombination and enhance the efficiency of energy trapping. Because the dark states cannot be populated by optical transitions from the ground state, they are usually accessed through phononic relaxation from the bright states. In this study, we explore a novel way of connecting the dark states and the bright states via optical transitions. In a ring-like chromophore system inspired by natural photosynthetic antennae, the single-excitation bright state can be optically connected to the lowest energy single-excitation dark state through certain double-excitation states. We call such double-excitation states the ferry states and show that they are the result of accidental degeneracy between two categories of double-excitation states. We then mathematically prove that the ferry states are only available when N, the number of subunits on the ring, satisfies N=4l+2 (l being an integer). Numerical calculations confirm that the ferry states enhance the energy transfer power of our model, showing a significant energy transfer power spike at N=6 compared with smaller N values, even without phononic relaxation. The proposed mathematical theory for the ferry states is not restricted to this one particular system or numerical model. In fact, it is potentially applicable to any coherent optical system that adopts a ring-shaped chromophore arrangement. Beyond the ideal case, the ferry state mechanism also demonstrates robustness under weak phononic dissipation, weak site energy disorder, and large coupling strength disorder

    Stochastic thermodynamics of rapidly driven systems

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    We present the stochastic thermodynamics analysis of an open quantum system weakly coupled to multiple reservoirs and driven by a rapidly oscillating external field. The analysis is built on a modified stochastic master equation in the Floquet basis. Transition rates are shown to satisfy the local detailed balance involving the entropy flowing out of the reservoirs. The first and second law of thermodynamics are also identified at the trajectory level. Mechanical work is identified by means of initial and final projections on energy eigenstates of the system. We explicitly show that this two step measurement becomes unnecessary in the long time limit. A steady-state fluctuation theorem for the currents and rate of mechanical work is also established. This relation does not require the introduction of a time reversed external driving which is usually needed when considering systems subjected to time asymmetric external fields. This is understood as a consequence of the secular approximation applied in consistency with the large time scale separation between the fast driving oscillations and the slower relaxation dynamics induced by the environment. Our results are finally illustrated on a model describing a thermodynamic engine.Comment: Equation (31) removed and subsequent discussion improved. References improved and minor corrections. v3: published versio

    Effects of Methylmercury on Notch Targets and Motor Nerve Development in Drosophila

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    Methylmercury (MeHg) is a ubiquitous environmental toxin. Exposure to MeHg in humans occurs primarily through the consumption of contaminated seafood. MeHg has been shown to act most strongly during neural development. Epidemiological data on the effect MeHg exposure through seafood has on children and fetuses is conflicted, with large cohort studies showing both presence and absence of MeHg-induced deficits in achieving developmental milestones. Because of this uncertainty in the literature it is important that we come to understand the mechanisms of MeHg toxicity so that we might advise the public more accurately on the risks of MeHg exposure. Research into the mechanisms of MeHg toxicity has found a number of cellular and molecular effects including disruptions of microtubule formation, Ca2+ homeostasis, and glutamate signaling. However, none of these effects of MeHg fully explains its neurodevelopmental specificity. Previous work in Drosophila neural-derived cell lines has shown that MeHg causes upregulation of the canonical Notch response gene E(spl)m . The Notch pathway is crucial to neural development and perturbation of a Notch target may explain the developmental specificity of MeHg. In this dissertation I describe experiments I performed to test the hypothesis that the observed upregulation of E(spl)m plays an important role in MeHg toxicity in Drosophila. I first describe experimental evidence that E(spl)m is upregulated by MeHg treatment in vivo in Drosophila embryos in addition to cells, as has previously been shown. By contrasting the effects of the toxic inorganic mercurial HgCl2 with MeHg I show that the E(spl)m expression response to MeHg is not simply a stress response and is a likely specific activity of MeHg. I also show that the effect of MeHg on E(spl)m expression is not simply due to a developmental delay induced by the toxin. I also identify two neural phenotypes of MeHg toxicity in Drosophila embryos, in the outgrowth of the intersegmental and segmental motor nerves. Genetic manipulation causing overactivity of the Notch pathway in neurons can mimic these phenotypes. However, induced expression of E(spl)m in neurons does not cause a failure of motor nerve outgrowth. Upon further examination I demonstrate that endogenous expression of E(spl)m occurs in the muscle. Induced E(spl)m expression in the muscle causes a segmental nerve phenotype similar to MeHg treatment, indicating a role for E(spl)m in MeHg toxicity in this system. MeHg treatment and E(spl)m overexpression in the muscle causes a failure of normal muscle development. Yet, this gross developmental abnormality only partially explains the observed motor nerve phenotype. E(spl)m is unique among the E(spl) genes in its ability to cause these muscle and motor nerve phenotypes as shown by contrasting genetic manipulation of the closely related E(spl)m . Overall my findings support the hypothesis that MeHg toxicity in Drosophila is mediated in part by E(spl)m . They also suggest that E(spl)m plays an important role in the formation of the muscle during embryonic development, contributing to the literature describing disparate functions for E(spl) genes despite structural similarities. Finally, my findings suggest that MeHg may be able to impact neural development through toxicity in supporting tissues rather than neurons themselves. This final finding has implications for the study of MeHg toxicity in humans, and is supported by previous findings that describe a role of glia in modulating MeHg neurotoxicity
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