22,313 research outputs found

    Scattering measurements on natural and model trees

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    The acoustical back scattering from a simple scale model of a tree has been experimentally measured. The model consisted of a trunk and six limbs, each with 4 branches; no foliage or twigs were included. The data from the anechoic chamber measurements were then mathematically combined to construct the effective back scattering from groups of trees. Also, initial measurements have been conducted out-of-doors on a single tree in an open field in order to characterize its acoustic scattering as a function of azimuth angle. These measurements were performed in the spring, prior to leaf development. The data support a statistical model of forest scattering; the scattered signal spectrum is highly irregular but with a remarkable general resemblance to the incident signal spectrum. Also, the scattered signal's spectra showed little dependence upon scattering angle

    Second-generation PLINK: rising to the challenge of larger and richer datasets

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    PLINK 1 is a widely used open-source C/C++ toolset for genome-wide association studies (GWAS) and research in population genetics. However, the steady accumulation of data from imputation and whole-genome sequencing studies has exposed a strong need for even faster and more scalable implementations of key functions. In addition, GWAS and population-genetic data now frequently contain probabilistic calls, phase information, and/or multiallelic variants, none of which can be represented by PLINK 1's primary data format. To address these issues, we are developing a second-generation codebase for PLINK. The first major release from this codebase, PLINK 1.9, introduces extensive use of bit-level parallelism, O(sqrt(n))-time/constant-space Hardy-Weinberg equilibrium and Fisher's exact tests, and many other algorithmic improvements. In combination, these changes accelerate most operations by 1-4 orders of magnitude, and allow the program to handle datasets too large to fit in RAM. This will be followed by PLINK 2.0, which will introduce (a) a new data format capable of efficiently representing probabilities, phase, and multiallelic variants, and (b) extensions of many functions to account for the new types of information. The second-generation versions of PLINK will offer dramatic improvements in performance and compatibility. For the first time, users without access to high-end computing resources can perform several essential analyses of the feature-rich and very large genetic datasets coming into use.Comment: 2 figures, 1 additional fil

    User-Fee Financing of USDA Meat and Poultry Inspection

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    USDA's Food Safety and Inspection Service (FSIS) finances about 13.5 percent of its budget outlays through user fees for overtime and unscheduled meat and poultry inspections. User fees play an increasingly important role in financing government programs, and FSIS has frequently requested expanded authority to charge user fees for more of its operations. Congress has consistently rejected the FSIS requests and has placed important restrictions on fees and the uses of fee revenue at those agencies that have been granted more extensive user fee authority. This report surveys the application of user-fees for financing meat and poultry inspection programs in other countries; reviews user-fee systems in other Federal agencies, particularly those with food and agricultural missions or regulatory responsibilities; and discusses the relevant economics literature on the use and design of user fees. Finally, we suggest several elements that should underlie the structure of user fees for meat and poultry inspection, should such a program be introduced. euser fees, meat inspection, public finance, Livestock Production/Industries, Public Economics,

    Deformation-Enhanced Fluctuations in the Red Cell Skeleton with Theoretical Relations to Elasticity, Connectivity, and Spectrin Unfolding

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    To assess local elasticity in the red cell’s spectrin-actin network, nano-particles were tethered to actin nodes and their constrained thermal motions were tracked. Cells were both immobilized and controllably deformed by aspiration into a micropipette. Since the network is well-appreciated as soft, thermal fluctuations even in an unstressed portion of network were expected to be many tens of nanometers based on simple equipartition ideas. Real-time particle tracking indeed reveals such root-mean-squared motions for 40-nm fluorescent beads either tethered to actin directly within a cell ghost or connected to actin from outside a cell via glycophorin. Moreover, the elastically constrained displacements are significant on the scale of the network’s internodal distance of ~60-80 nm. Surprisingly, along the aspirated projection—where the network is axially extended by as much as twofold or more—fluctuations in the axial direction are increased by almost twofold relative to motions in the unstressed network. The molecular basis for such strain softening is discussed broadly in terms of force-driven transitions. Specific considerations are given to 1) protein dissociations that reduce network connectivity, and 2) unfolding kinetics of a localized few of the red cell’s ~107 spectrin repeats

    Impacts of membrane biophysics in Alzheimer’s disease: from amyloid precursor protein processing to Aβ peptide-induced membrane changes

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    An increasing amount of evidence supports the notion that cytotoxic effects of amyloid-β peptide (Aβ), the main constituent of senile plaques in Alzheimer’s disease (AD), are strongly associated with its ability to interact with membranes of neurons and other cerebral cells. Aβ is derived from amyloidogenic cleavage of amyloid precursor protein (AβPP) by β- and γ-secretase. In the nonamyloidogenic pathway, AβPP is cleaved by α-secretases. These two pathways compete with each other, and enhancing the non-amyloidogenic pathway has been suggested as a potential pharmacological approach for the treatment of AD. Since AβPP, α-, β-, and γ-secretases are membrane-associated proteins, AβPP processing and Aβ production can be affected by the membrane composition and properties. There is evidence that membrane composition and properties, in turn, play a critical role in Aβ cytotoxicity associated with its conformational changes and aggregation into oligomers and fibrils. Understanding themechanisms leading to changes in a membrane’s biophysical properties and how they affect AβPP processing and Aβ toxicity should prove to provide new therapeutic strategies for prevention and treatment of AD

    Membrane biophysics and mechanics in Alzheimer's disease

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    Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Aβ can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Aβ on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions

    Membrane biophysics and mechanics in Alzheimer's disease

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    Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Aβ can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Aβ on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions

    Impacts of Membrane Biophysics in Alzheimer's Disease: From Amyloid Precursor Protein Processing to Aβ Peptide-Induced Membrane Changes

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    An increasing amount of evidence supports the notion that cytotoxic effects of amyloid-β peptide (Aβ), the main constituent of senile plaques in Alzheimer's disease (AD), are strongly associated with its ability to interact with membranes of neurons and other cerebral cells. Aβ is derived from amyloidogenic cleavage of amyloid precursor protein (AβPP) by β- and γ-secretase. In the nonamyloidogenic pathway, AβPP is cleaved by α-secretases. These two pathways compete with each other, and enhancing the non-amyloidogenic pathway has been suggested as a potential pharmacological approach for the treatment of AD. Since AβPP, α-, β-, and γ-secretases are membrane-associated proteins, AβPP processing and Aβ production can be affected by the membrane composition and properties. There is evidence that membrane composition and properties, in turn, play a critical role in Aβ cytotoxicity associated with its conformational changes and aggregation into oligomers and fibrils. Understanding the mechanisms leading to changes in a membrane's biophysical properties and how they affect AβPP processing and Aβ toxicity should prove to provide new therapeutic strategies for prevention and treatment of AD

    Chapman-Enskog expansion about nonequilibrium states: the sheared granular fluid

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    The Chapman-Enskog method of solution of kinetic equations, such as the Boltzmann equation, is based on an expansion in gradients of the deviations fo the hydrodynamic fields from a uniform reference state (e.g., local equilibrium). This paper presents an extension of the method so as to allow for expansions about \emph{arbitrary}, far-from equilibrium reference states. The primary result is a set of hydrodynamic equations for studying variations from the arbitrary reference state which, unlike the usual Navier-Stokes hydrodynamics, does not restrict the reference state in any way. The method is illustrated by application to a sheared granular gas which cannot be studied using the usual Navier-Stokes hydrodynamics.Comment: 23 pages, no figures. Submited to PRE Replaced to correct misc. errors Replaced to correct misc. errors, make notation more consistant, extend discussio
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