152 resultados para Dendrite Coherency
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The dendrite coherency point of Al-Si-Cu alloys was determined by thermal analysis and rheological measurement methods by performing parallel measurements at two cooling rates for aluminum alloys across a wide range of silicon and copper contents. Contrary to previous findings, the two methods yield significantly different values for the fraction solid at the dendrite coherency point. This disparity is greatest for alloys of low solute concentration. The results from this study also contradict previously reported tl ends in the effect of cooling rate on the dendritic coherency point. Consideration of the results shows that thermal analysis is not a valid technique for the measurement of coherency. Analysis of the results from rheological testing indicates that silicon concentration has a dominant effect on grain size and dendritic morphology, independent of cooling rate and copper content, and thus is the factor that determines the fraction solid at dendrite coherency for Al-Si-Cu alloys.
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A new conceptual framework has been developed which explains the formation of shear-related casting defects such as porosity, segregation and tears. The theory relates defect formation to the mechanical behaviour of the partially solidified microstructure when shear stresses are developed during the filling of a casting and by the subsequent feeding processes during solidification. Two transition points, the dendrite coherency point and the maximum packing solid fraction, divide the mushy zone into three regions of different mechanical and feeding behaviours. The response of the mush to shear is related to the presence of these zones during solidification of a casting. The resulting defects are rationalized by considering the governing local shear stress and shear rate, local strength and time available for fluid flow. The design of the casting, the casting process used and the alloy composition all influence the relative importance of shearing on defect formation. (C) 1998 Acta Metallurgica Inc. Published by Elsevier Science Ltd. All rights reserved.
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An analytical approach to the stress development in the coherent dendritic network during solidification is proposed. Under the assumption that stresses are developed in the network as a result of the friction resisting shrinkage-induced interdendritic fluid flow, the model predicts the stresses in the solid. The calculations reflect the expected effects of postponed dendrite coherency, slower solidification conditions, and variations of eutectic volume fraction and shrinkage. Comparing the calculated stresses to the measured shear strength of equiaxed mushy zones shows that it is possible for the stresses to exceed the strength, thereby resulting in reorientation or collapse of the dendritic network.
A rheological assessment of the effect of trace level Ni additions on the solidification of Sn-0.7Cu
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The influence of trace level Ni additions on the eutectic solidification mode of Sn-0.7Cu has been studied using continuous torque experiments during solidification. The solid fraction at which resistance to paddle rotation at the thermal centre of the sample occurs is related to the spatial distribution of solid during solidification. The results indicate that a transition in solidification mode occurs in the range 0-300 ppm Ni. Growth occurs antiparallel to heat flow from near the mould walls in the Ni-free alloy, while equiaxed growth from distributed centres dominates in alloys containing at least 300 ppm Ni. (c) 2006 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
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Shrinkage porosity as a volume change related casting defect in lamellar cast iron was reported in theliterature to form during solidification in connection to the dendrite coherency. The present work includesan experimental study on dendrite coherency – also called columnar-to-equiaxed transition in lamellar castiron using thermal analysis and expansion force measurements. Investigation was carried out in order tostudy the mechanism of dendrite coherency formation. Cylindrical test bars were cast from the same alloywith different pouring temperature, amount of inoculant and time between the addition of inoculant andstart of pouring the samples. Cooling rate and expansion force was recorded as a function of time. Anumerical algorithm based on temperature differences measured under solidification was used to inter-pret the solidification process. Three different methods have been compared to determine the columnarto equiaxed transition. The compared methods were based on registered temperature differences, basedon registered expansion forces during the volume change of the solidifying samples and based on the cal-culated released latent heat of crystallization. The obtained results indicate a considerable influence on theformation and progress of coherency due to variation of casting parameters. It has been shown that thecoherency is not a single event at a defined time moment rather a process progressing during a timeinterval.
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A comprehensive probabilistic model for simulating dendrite morphology and investigating dendritic growth kinetics during solidification has been developed, based on a modified Cellular Automaton (mCA) for microscopic modeling of nucleation, growth of crystals and solute diffusion. The mCA model numerically calculated solute redistribution both in the solid and liquid phases, the curvature of dendrite tips and the growth anisotropy. This modeling takes account of thermal, curvature and solute diffusion effects. Therefore, it can simulate microstructure formation both on the scale of the dendrite tip length. This model was then applied for simulating dendritic solidification of an Al-7%Si alloy. Both directional and equiaxed dendritic growth has been performed to investigate the growth anisotropy and cooling rate on dendrite morphology. Furthermore, the competitive growth and selection of dendritic crystals have also investigated.
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The role of ubiquitin in development of the mammalian brain has been studied using a monoclonal antibody, RHUb1, specific for ubiquitin. Immunodevelopment of western blots of homogenate samples of the cerebral cortex, hippocampus and cerebellum prepared from animals of known postnatal age show marked developmental changes in conjugate level. Striking decreases in the level of a prominent conjugate of molecular weight 22,000, which is identified as ubiquitinated histone, are observed during the first postnatal week in the cerebral cortex and hippocampus, but not the cerebellum. A marked overall developmental decrease in the level of high-molecular-weight (> 40,000) ubiquitin conjugates which occurs predominantly during the third, but also the fourth, postnatal week is observed in all three regions. Immunocytochemical data obtained with the RHUb1 antibody show intense staining of neuronal perikarya, nuclei and dendrites in early postnatal cerebral cortex and hippocampus. Staining of pyramidal cell perikarya and dendrites is particularly prominent. The intensity of dendritic staining, particularly for the cerebral cortex, shows a striking decrease after postnatal day 14 and only faint dendritic staining is observed in the adult. In early postnatal cerebellum, immunoreactivity is predominantly nuclear, though some staining of the proximal regions of Purkinje cell dendrites is observed between postnatal days 4 and 19. As with the cerebral cortex and hippocampus, most of the ubiquitin reactivity is lost in adult animals. The loss of dendritic staining, particularly in the cerebral cortex, correlates with the decrease in the level of high-molecular-weight ubiquitin conjugates observed on the western blots. Immunodevelopment of western blots of a range of subcellular fractions prepared from developing rat forebrain shows that the developmental decrease in the level of high-molecular-weight ubiquitin conjugates is not uniform for all fractions. The decrease in conjugate level is most marked for the cell-soluble, mitochondrial and detergent-insoluble cytoskeletal fractions. Taken overall, the data suggest a role for ubiquitin in dendrite outgrowth and arborization, loss of dendritic ubiquitin immunoreactivity correlating with completion of these processes.
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In this paper, we present a comprehensive study of different Independent Component Analysis (ICA) algorithms for the calculation of coherency and sharpness of electroencephalogram (EEG) signals, in order to investigate the possibility of early detection of Alzheimer’s disease (AD). We found that ICA algorithms can help in the artifact rejection and noise reduction, improving the discriminative property of features in high frequency bands (specially in high alpha and beta ranges). In addition to different ICA algorithms, the optimum number of selected components is investigated, in order to help decision processes for future works.
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JNK1 is a MAP-kinase that has proven a significant player in the central nervous system. It regulates brain development and the maintenance of dendrites and axons. Several novel phosphorylation targets of JNK1 were identified in a screen performed in the Coffey lab. These proteins were mainly involved in the regulation of neuronal cytoskeleton, influencing the dynamics and stability of microtubules and actin. These structural proteins form the dynamic backbone for the elaborate architecture of the dendritic tree of a neuron. The initiation and branching of the dendrites requires a dynamic interplay between the cytoskeletal building blocks. Both microtubules and actin are decorated by associated proteins which regulate their dynamics. The dendrite-specific, high molecular weight microtubule associated protein 2 (MAP2) is an abundant protein in the brain, the binding of which stabilizes microtubules and influences their bundling. Its expression in non-neuronal cells induces the formation of neurite-like processes from the cell body, and its function is highly regulated by phosphorylation. JNK1 was shown to phosphorylate the proline-rich domain of MAP2 in vivo in a previous study performed in the group. Here we verify three threonine residues (T1619, T1622 and T1625) as JNK1 targets, the phosphorylation of which increases the binding of MAP2 to microtubules. This binding stabilizes the microtubules and increases process formation in non-neuronal cells. Phosphorylation-site mutants were engineered in the lab. The non-phosphorylatable mutant of MAP2 (MAP2- T1619A, T1622A, T1625A) in these residues fails to bind microtubules, while the pseudo-phosphorylated form, MAP2- T1619D, T1622D, Thr1625D, efficiently binds and induces process formation even without the presence of active JNK1. Ectopic expression of the MAP2- T1619D, T1622D, Thr1625D in vivo in mouse brain led to a striking increase in the branching of cortical layer 2/3 (L2/3) pyramidal neurons, compared to MAP2-WT. The dendritic complexity defines the receptive field of a neuron and dictates the output to the postsynaptic cells. Previous studies in the group indicated altered dendrite architecture of the pyramidal neurons in the Jnk1-/- mouse motor cortex. Here, we used Lucifer Yellow loading and Sholl analysis of neurons in order to study the dendritic branching in more detail. We report a striking, opposing effect in the absence of Jnk1 in the cortical layers 2/3 and 5 of the primary motor cortex. The basal dendrites of pyramidal neurons close to the pial surface at L2/3 show a reduced complexity. In contrast, the L5 neurons, which receive massive input from the L2/3 neurons, show greatly increased branching. Another novel substrate identified for JNK1 was MARCKSL1, a protein that regulates actin dynamics. It is highly expressed in neurons, but also in various cancer tissues. Three phosphorylation target residues for JNK1 were identified, and it was demonstrated that their phosphorylation reduces actin turnover and retards migration of these cells. Actin is the main cytoskeletal component in dendritic spines, the site of most excitatory synapses in pyramidal neurons. The density and gross morphology of the Lucifer Yellow filled dendrites were characterized and we show reduced density and altered morphology of spines in the motor cortex and in the hippocampal area CA3. The dynamic dendritic spines are widely considered to function as the cellular correlate during learning. We used a Morris water maze to test spatial memory. Here, the wild-type mice outperformed the knock-out mice during the acquisition phase of the experiment indicating impaired special memory. The L5 pyramidal neurons of the motor cortex project to the spinal cord and regulate the movement of distinct muscle groups. Thus the altered dendrite morphology in the motor cortex was expected to have an effect on the input-output balance in the signaling from the cortex to the lower motor circuits. A battery of behavioral tests were conducted for the wild-type and Jnk1-/- mice, and the knock-outs performed poorly compared to wild-type mice in tests assessing balance and fine motor movements. This study expands our knowledge of JNK1 as an important regulator of the dendritic fields of neurons and their manifestations in behavior.
Models of passive and active dendrite motoneuron pools and their differences in muscle force control
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Motoneuron (MN) dendrites may be changed from a passive to an active state by increasing the levels of spinal cord neuromodulators, which activate persistent inward currents (PICs). These exert a powerful influence on MN behavior and modify the motor control both in normal and pathological conditions. Motoneuronal PICs are believed to induce nonlinear phenomena such as the genesis of extra torque and torque hysteresis in response to percutaneous electrical stimulation or tendon vibration in humans. An existing large-scale neuromuscular simulator was expanded to include MN models that have a capability to change their dynamic behaviors depending on the neuromodulation level. The simulation results indicated that the variability (standard deviation) of a maintained force depended on the level of neuromodulatory activity. A force with lower variability was obtained when the motoneuronal network was under a strong influence of PICs, suggesting a functional role in postural and precision tasks. In an additional set of simulations when PICs were active in the dendrites of the MN models, the results successfully reproduced experimental results reported from humans. Extra torque was evoked by the self-sustained discharge of spinal MNs, whereas differences in recruitment and de-recruitment levels of the MNs were the main reason behind torque and electromyogram (EMG) hysteresis. Finally, simulations were also used to study the influence of inhibitory inputs on a MN pool that was under the effect of PICs. The results showed that inhibition was of great importance in the production of a phasic force, requiring a reduced co-contraction of agonist and antagonist muscles. These results show the richness of functionally relevant behaviors that can arise from a MN pool under the action of PICs.
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We report that fast (mainly 30- to 40-Hz) coherent electric field oscillations appear spontaneously during brain activation, as expressed by electroencephalogram (EEG) rhythms, and they outlast the stimulation of mesopontine cholinergic nuclei in acutely prepared cats. The fast oscillations also appear during the sleep-like EEG patterns of ketamine/xylazine anesthesia, but they are selectively suppressed during the prolonged phase of the slow (<1-Hz) sleep oscillation that is associated with hyperpolarization of cortical neurons. The fast (30- to 40-Hz) rhythms are synchronized intracortically within vertical columns, among closely located cortical foci, and through reciprocal corticothalamic networks. The fast oscillations do not reverse throughout the depth of the cortex. This aspect stands in contrast with the conventional depth profile of evoked potentials and slow sleep oscillations that display opposite polarity at the surface and midlayers. Current-source-density analyses reveal that the fast oscillations are associated with alternating microsinks and microsources across the cortex, while the evoked potentials and the slow oscillation display a massive current sink in midlayers, confined by two sources in superficial and deep layers. The synchronization of fast rhythms and their high amplitudes indicate that the term "EEG desynchronization," used to designate brain-aroused states, is incorrect and should be replaced with the original term, "EEG activation" [Moruzzi, G. & Magoun, H.W. (1949) Electroencephalogr. Clin. Neurophysiol. 1, 455-473].
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Thesis (Ph.D.)--University of Washington, 2016-06
Terrain classification based on markov random field texture modeling of SAR and SAR coherency images
Direct measurement of coherency limits for strain relaxation in heteroepitaxial core/shell nanowires
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The growth of heteroepitaxially strained semiconductors at the nanoscale enables tailoring of material properties for enhanced device performance. For core/shell nanowires (NWs), theoretical predictions of the coherency limits and the implications they carry remain uncertain without proper identification of the mechanisms by which strains relax. We present here for the Ge/Si core/shell NW system the first experimental measurement of critical shell thickness for strain relaxation in a semiconductor NW heterostructure and the identification of the relaxation mechanisms. Axial and tangential strain relief is initiated by the formation of periodic a/2 〈110〉 perfect dislocations via nucleation and glide on {111} slip-planes. Glide of dislocation segments is directly confirmed by real-time in situ transmission electron microscope observations and by dislocation dynamics simulations. Further shell growth leads to roughening and grain formation which provides additional strain relief. As a consequence of core/shell strain sharing in NWs, a 16 nm radius Ge NW with a 3 nm Si shell is shown to accommodate 3% coherent strain at equilibrium, a factor of 3 increase over the 1 nm equilibrium critical thickness for planar Si/Ge heteroepitaxial growth. © 2012 American Chemical Society.