1,996 research outputs found

    Dendritic to globular morphology transition in ternary alloy solidification

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    The evolution of solidification microstructures in ternary metallic alloys is investigated by adaptive finite element simulations of a general multicomponent phase-field model. A morphological transition from dendritic to globular growth is found by varying the alloy composition at a fixed undercooling. The dependence of the growth velocity and of the impurity segregation in the solid phase on the composition is analyzed and indicates a smooth type of transition between the dendritic and globular growth structures.Comment: 4 pages, 2 figure

    Phase Field Modeling of Fracture and Stress Induced Phase Transitions

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    We present a continuum theory to describe elastically induced phase transitions between coherent solid phases. In the limit of vanishing elastic constants in one of the phases, the model can be used to describe fracture on the basis of the late stage of the Asaro-Tiller-Grinfeld instability. Starting from a sharp interface formulation we derive the elastic equations and the dissipative interface kinetics. We develop a phase field model to simulate these processes numerically; in the sharp interface limit, it reproduces the desired equations of motion and boundary conditions. We perform large scale simulations of fracture processes to eliminate finite-size effects and compare the results to a recently developed sharp interface method. Details of the numerical simulations are explained, and the generalization to multiphase simulations is presented

    Modeling fracture cementation processes in calcite limestone: a phase-field study

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    The present work investigates the influence of crack opening rates on the development of four important calcite vein morphologies, namely fibrous, elongate-blocky, partially open, and euhedral, as a result of bitaxial growth in syntaxial veins using a multiphase-field model. The continued fracturing that occurs during synkinematic cementation in these veins is simulated using the geometric shift algorithm. The stark resemblance of the numerically sealed vein microstructures with the natural samples in terms of structural characteristics as well as remaining pore space signifies a dominant role of crack opening rates in the resulting morphological patterns. Further, simulation results of slow crack opening rates reveal that non-uniform fibers of variable lengths are formed when initial crack aperture is small, due to suppression of growth competition and vice versa

    Calibrating micro-computed tomography data to permeability experiments and petrography – insights from Digital Rocks

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    Petrophysical measurements on core plugs integrated with petrographic information from thin-sections are established methods in reservoir quality assessment. X-ray micro-computed tomography (μCT) presents an opportunity to derive the internal structure of reservoir sandstones for digital fluid flow simulations, while si-multaneously assessing mineral distribution in 3D based on mineral densities. We compare the sin-gle-phase permeabilities obtained with fluid flow sim-ulations and experiments and discuss the anisotropic nature of the permeability tensor in both single- and two-phase flow. The results demonstrate a closer match for μCT porosity to petrophysical porosity com-pared to optical porosity, and an acceptable first order fit of the main mineralogical constituents. One-phase fluid flow simulations deliver results within 10–20 % of the laboratory measurements. Two-phase flow sim-ulations enable the assessment of relative permeabili-ties in rocks with water-sensitive minerals. However, μCT-based fluid flow simulations are computationally very demanding and time consuming due to the heter-ogeneous nature of natural sandstone samples, and require a tradeoff between resolution, representative volume, and cost. Rock composition reconstructed from μCT images can be used as a first-order approxi-mation for the composition of a sample, but is unable to confidently identify minerals that occur in minor quantities due to constraints of the chosen resolution. Thus, sandstone analyses by μCT cannot completely replace established methods

    Microstructure simulations

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    Coniferous bark hot steam treatment for the elimination of the pinewood nematode

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    In order to develop an artificial heat treatment to eliminate the pinewood nematode (PWN), Bursaphelenchus xylophilus, from coniferous bark, an industrial equipment, based on hot steam was build up which enables continuous bark treatment for more than 30 min with temperatures above 80ºC. Biological assays were performed using experimental units (bags) with Pinus pinaster bark and wood chips containing more than 100 000 PWN (.60% third dispersal juvenile s tage). The bags were heat treated for 30 min and the temperature inside monitored by temperature probes. The total number of live nematodes was quantified immediately after treatment and after incubation (25ºC for 15 days) and in both situations no nematodes were detected revealing efficacy in eliminating PWN from coniferous bark

    Epigenetic suppression of hippocampal calbindin-D28k by ΔFosB drives seizure-related cognitive deficits.

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    The calcium-binding protein calbindin-D28k is critical for hippocampal function and cognition, but its expression is markedly decreased in various neurological disorders associated with epileptiform activity and seizures. In Alzheimer\u27s disease (AD) and epilepsy, both of which are accompanied by recurrent seizures, the severity of cognitive deficits reflects the degree of calbindin reduction in the hippocampal dentate gyrus (DG). However, despite the importance of calbindin in both neuronal physiology and pathology, the regulatory mechanisms that control its expression in the hippocampus are poorly understood. Here we report an epigenetic mechanism through which seizures chronically suppress hippocampal calbindin expression and impair cognition. We demonstrate that ΔFosB, a highly stable transcription factor, is induced in the hippocampus in mouse models of AD and seizures, in which it binds and triggers histone deacetylation at the promoter of the calbindin gene (Calb1) and downregulates Calb1 transcription. Notably, increasing DG calbindin levels, either by direct virus-mediated expression or inhibition of ΔFosB signaling, improves spatial memory in a mouse model of AD. Moreover, levels of ΔFosB and calbindin expression are inversely related in the DG of individuals with temporal lobe epilepsy (TLE) or AD and correlate with performance on the Mini-Mental State Examination (MMSE). We propose that chronic suppression of calbindin by ΔFosB is one mechanism through which intermittent seizures drive persistent cognitive deficits in conditions accompanied by recurrent seizures

    ΔFosB Regulates Gene Expression and Cognitive Dysfunction in a Mouse Model of Alzheimer\u27s Disease.

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    Alzheimer\u27s disease (AD) is characterized by cognitive decline and 5- to 10-fold increased seizure incidence. How seizures contribute to cognitive decline in AD or other disorders is unclear. We show that spontaneous seizures increase expression of ΔFosB, a highly stable Fos-family transcription factor, in the hippocampus of an AD mouse model. ΔFosB suppressed expression of the immediate early gene c-Fos, which is critical for plasticity and cognition, by binding its promoter and triggering histone deacetylation. Acute histone deacetylase (HDAC) inhibition or inhibition of ΔFosB activity restored c-Fos induction and improved cognition in AD mice. Administration of seizure-inducing agents to nontransgenic mice also resulted in ΔFosB-mediated suppression of c-Fos, suggesting that this mechanism is not confined to AD mice. These results explain observations that c-Fos expression increases after acute neuronal activity but decreases with chronic activity. Moreover, these results indicate a general mechanism by which seizures contribute to persistent cognitive deficits, even during seizure-free periods

    Distinct sites of opiate reward and aversion within the midbrain identified using a herpes simplex virus vector expressing GluR1

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    Repeated administration of morphine increases expression of GluR1 (an AMPA glutamate receptor subunit) in the ventral tegmental area (VTA) of the midbrain, an important neural substrate for the rewarding actions of morphine. Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. We now report that in rats given HSV-GluR1 directly into the VTA, morphine is most rewarding when maximal transgene expression is in the rostral VTA, whereas morphine is aversive when maximal transgene expression is in the caudal VTA. Dual-labeling immunohistochemistry shows that this difference cannot be explained by a different fraction of dopaminergic neurons infected in the rostral versus caudal VTA. No such anatomical specificity is seen in rats given VTA microinjections of HSV-LacZ, a vector expressing a control protein (beta-galactosidase). These results suggest that distinct substrates within the VTA itself differentially contribute to the rewarding and aversive properties of opiates

    The effect of compression shock heating in collision welding

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    This work discusses the origin of temperature rise during the collision welding process. The different physical irreversible and reversible mechanisms which act as heat sources are described: isentropic compression work, shock dissipation, plasticity, and phase transitions. The temperature increase due to these effects is quantified in a continuum mechanics approach, and compared to predictions of atomistic molecular dynamics simulations. Focusing on a single impact scenario of 1100 aluminium at 700 m/s, our results indicate that shock heating and plastic work only effect a temperature rise of 100 K, and that the effects of phase change are not significant. This temperature rise cannot explain welding. In consequence, the relevant mechanism which effects bonding in collision welding must be due to the jet, which is only formed at oblique impact angles
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