Relevant bibliographies by topics / Dendrite development

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Academic literature on the topic 'Dendrite development'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dendrite development"

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Leonard, Carrie E., Maryna Baydyuk, Marissa A. Stepler, Denver A. Burton, and Maria J. Donoghue. "EphA7 isoforms differentially regulate cortical dendrite development." PLOS ONE 15, no. 12 (2020): e0231561. http://dx.doi.org/10.1371/journal.pone.0231561.

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The shape of a neuron facilitates its functionality within neural circuits. Dendrites integrate incoming signals from axons, receiving excitatory input onto small protrusions called dendritic spines. Therefore, understanding dendritic growth and development is fundamental for discerning neural function. We previously demonstrated that EphA7 receptor signaling during cortical development impacts dendrites in two ways: EphA7 restricts dendritic growth early and promotes dendritic spine formation later. Here, the molecular basis for this shift in EphA7 function is defined. Expression analyses reveal that EphA7 full-length (EphA7-FL) and truncated (EphA7-T1; lacking kinase domain) isoforms are dynamically expressed in the developing cortex. Peak expression of EphA7-FL overlaps with dendritic elaboration around birth, while highest expression of EphA7-T1 coincides with dendritic spine formation in early postnatal life. Overexpression studies in cultured neurons demonstrate that EphA7-FL inhibits both dendritic growth and spine formation, while EphA7-T1 increases spine density. Furthermore, signaling downstream of EphA7 shifts during development, such that in vivo inhibition of mTOR by rapamycin in EphA7-mutant neurons ameliorates dendritic branching, but not dendritic spine phenotypes. Finally, direct interaction between EphA7-FL and EphA7-T1 is demonstrated in cultured cells, which results in reduction of EphA7-FL phosphorylation. In cortex, both isoforms are colocalized to synaptic fractions and both transcripts are expressed together within individual neurons, supporting a model where EphA7-T1 modulates EphA7-FL repulsive signaling during development. Thus, the divergent functions of EphA7 during cortical dendrite development are explained by the presence of two variants of the receptor.
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Ehlers, Michael D. "Dendrite development." Journal of Cell Biology 170, no. 4 (2005): 517–19. http://dx.doi.org/10.1083/jcb.200507096.

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Kalb, R. G. "Regulation of motor neuron dendrite growth by NMDA receptor activation." Development 120, no. 11 (1994): 3063–71. http://dx.doi.org/10.1242/dev.120.11.3063.

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Spinal motor neurons undergo great changes in morphology, electrophysiology and molecular composition during development. Some of this maturation occurs postnatally when limbs are employed for locomotion, suggesting that neuronal activity may influence motor neuron development. To identify features of motor neurons that might be regulated by activity we first examined the structural development of the rat motor neuron cell body and dendritic tree labeled with cholera toxin-conjugated horseradish peroxidase. The motor neuron cell body and dendrites in the radial and rostrocaudal axes grew progressively over the first month of life. In contrast, the growth of the dendritic arbor/cell and number of dendritic branches was biphasic with overabundant growth followed by regression until the adult pattern was achieved. We next examined the influence of neurotransmission on the development of these motor neuron features. We found that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor inhibited cell body growth and dendritic branching in early postnatal life but had no effect on the maximal extent of dendrite growth in the radial and rostrocaudal axes. The effects of NMDA receptor antagonism on motor neurons and their dendrites was temporally restricted; all of our anatomic measures of dendrite structure were resistant to NMDA receptor antagonism in adults. These results suggest that the establishment of mature motor neuron dendritic architecture results in part from dendrite growth in response to afferent input during a sensitive period in early postnatal life.
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Sharp, D. J., W. Yu, and P. W. Baas. "Transport of dendritic microtubules establishes their nonuniform polarity orientation." Journal of Cell Biology 130, no. 1 (1995): 93–103. http://dx.doi.org/10.1083/jcb.130.1.93.

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The immature processes that give rise to both axons and dendrites contain microtubules (MTs) that are uniformly oriented with their plus-ends distal to the cell body, and this pattern is preserved in the developing axon. In contrast, developing dendrites gradually acquire nonuniform MT polarity orientation due to the addition of a subpopulation of oppositely oriented MTs (Baas, P. W., M. M. Black, and G. A. Banker. 1989. J. Cell Biol. 109:3085-3094). In theory, these minus-end-distal MTs could be locally nucleated and assembled within the dendrite itself, or could be transported into the dendrite after their nucleation within the cell body. To distinguish between these possibilities, we exposed cultured hippocampal neurons to nanomolar levels of vinblastine after one of the immature processes had developed into the axon but before the others had become dendrites. At these levels, vinblastine acts as a kinetic stabilizer of MTs, inhibiting further assembly while not substantially depolymerizing existing MTs. This treatment did not abolish dendritic differentiation, which occurred in timely fashion over the next two to three days. The resulting dendrites were flatter and shorter than controls, but were identifiable by their ultrastructure, chemical composition, and thickened tapering morphology. The growth of these dendrites was accompanied by a diminution of MTs from the cell body, indicating a net transfer of MTs from one compartment into the other. During this time, minus-end-distal microtubules arose in the experimental dendrites, indicating that new MT assembly is not required for the acquisition of nonuniform MT polarity orientation in the dendrite. Minus-end-distal microtubules predominated in the more proximal region of experimental dendrites, indicating that most of the MTs at this stage of development are transported into the dendrite with their minus-ends leading. These observations indicate that transport of MTs from the cell body is an essential feature of dendritic development, and that this transport establishes the nonuniform polarity orientation of MTs in the dendrite.
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Ligon, Cheryl, Eunju Seong, Ethan J. Schroeder та ін. "δ-Catenin engages the autophagy pathway to sculpt the developing dendritic arbor". Journal of Biological Chemistry 295, № 32 (2020): 10988–1001. http://dx.doi.org/10.1074/jbc.ra120.013058.

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The development of the dendritic arbor in pyramidal neurons is critical for neural circuit function. Here, we uncovered a pathway in which δ-catenin, a component of the cadherin–catenin cell adhesion complex, promotes coordination of growth among individual dendrites and engages the autophagy mechanism to sculpt the developing dendritic arbor. Using a rat primary neuron model, time-lapse imaging, immunohistochemistry, and confocal microscopy, we found that apical and basolateral dendrites are coordinately sculpted during development. Loss or knockdown of δ-catenin uncoupled this coordination, leading to retraction of the apical dendrite without altering basolateral dendrite dynamics. Autophagy is a key cellular pathway that allows degradation of cellular components. We observed that the impairment of the dendritic arbor resulting from δ-catenin knockdown could be reversed by knockdown of autophagy-related 7 (ATG7), a component of the autophagy machinery. We propose that δ-catenin regulates the dendritic arbor by coordinating the dynamics of individual dendrites and that the autophagy mechanism may be leveraged by δ-catenin and other effectors to sculpt the developing dendritic arbor. Our findings have implications for the management of neurological disorders, such as autism and intellectual disability, that are characterized by dendritic aberrations.
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Ybarra, Natividad, Peter J. Hemond, Michael P. O'Boyle, and Kelly J. Suter. "Spatially Selective, Testosterone-Independent Remodeling of Dendrites in Gonadotropin-Releasing Hormone (GnRH) Neurons Prepubertally in Male Rats." Endocrinology 152, no. 5 (2011): 2011–19. http://dx.doi.org/10.1210/en.2010-0871.

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Adult GnRH neurons exhibit a stereotypic morphology with a small soma, single axon, and single dendrite arising from the soma with little branching. The adult morphology of GnRH neurons in mice reflects an anatomical consolidation of dendrites over postnatal development. We examined this issue in rat GnRH neurons with biocytin filling in live hypothalamic slices from infant males, as adult littermates and in gonad-intact males, castrated males, and in males with one of three levels of testosterone (T) treatment. Somatic area and total dendritic length were significantly greater in infant males than in adults. Moreover, total numbers of dendrite branches were greater in infant males as compared with adults. The number of higher order branches and the lengths of higher order branches were also greater in infant males than in adults. Most interestingly, in adults a single dendrite arose from the somata, consistently at 180° from the axon. In contrast, prepubertal animals had an average of 2.2 ± 0.2 primary dendrites arising from somata (range, one to seven primary dendrites). Angles relative to the axon at which dendrites in prepubertal males emanated from GnRH somata were highly variable. Castration at 25 d of age and castration at 25 d of age with one of three levels of T treatment did not influence morphological parameters when GnRH neurons were examined between 40 d and 48 d of age. Thus, a spatially selective remodeling of primary dendrites and consolidation of distal GnRH dendritic arbors occurs during postnatal development and is largely independent of T.
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Takano, Tetsuya, Tomoki Urushibara, Nozomu Yoshioka, et al. "LMTK1 regulates dendritic formation by regulating movement of Rab11A-positive endosomes." Molecular Biology of the Cell 25, no. 11 (2014): 1755–68. http://dx.doi.org/10.1091/mbc.e14-01-0675.

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Neurons extend two types of neurites—axons and dendrites—that differ in structure and function. Although it is well understood that the cytoskeleton plays a pivotal role in neurite differentiation and extension, the mechanisms by which membrane components are supplied to growing axons or dendrites is largely unknown. We previously reported that the membrane supply to axons is regulated by lemur kinase 1 (LMTK1) through Rab11A-positive endosomes. Here we investigate the role of LMTK1 in dendrite formation. Down-regulation of LMTK1 increases dendrite growth and branching of cerebral cortical neurons in vitro and in vivo. LMTK1 knockout significantly enhances the prevalence, velocity, and run length of anterograde movement of Rab11A-positive endosomes to levels similar to those expressing constitutively active Rab11A-Q70L. Rab11A-positive endosome dynamics also increases in the cell body and growth cone of LMTK1-deficient neurons. Moreover, a nonphosphorylatable LMTK1 mutant (Ser34Ala, a Cdk5 phosphorylation site) dramatically promotes dendrite growth. Thus LMTK1 negatively controls dendritic formation by regulating Rab11A-positive endosomal trafficking in a Cdk5-dependent manner, indicating the Cdk5-LMTK1-Rab11A pathway as a regulatory mechanism of dendrite development as well as axon outgrowth.
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Feng, Chengye, Pankajam Thyagarajan, Matthew Shorey, et al. "Patronin-mediated minus end growth is required for dendritic microtubule polarity." Journal of Cell Biology 218, no. 7 (2019): 2309–28. http://dx.doi.org/10.1083/jcb.201810155.

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Microtubule minus ends are thought to be stable in cells. Surprisingly, in Drosophila and zebrafish neurons, we observed persistent minus end growth, with runs lasting over 10 min. In Drosophila, extended minus end growth depended on Patronin, and Patronin reduction disrupted dendritic minus-end-out polarity. In fly dendrites, microtubule nucleation sites localize at dendrite branch points. Therefore, we hypothesized minus end growth might be particularly important beyond branch points. Distal dendrites have mixed polarity, and reduction of Patronin lowered the number of minus-end-out microtubules. More strikingly, extra Patronin made terminal dendrites almost completely minus-end-out, indicating low Patronin normally limits minus-end-out microtubules. To determine whether minus end growth populated new dendrites with microtubules, we analyzed dendrite development and regeneration. Minus ends extended into growing dendrites in the presence of Patronin. In sum, our data suggest that Patronin facilitates sustained microtubule minus end growth, which is critical for populating dendrites with minus-end-out microtubules.
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Grueber, Wesley B., Lily Y. Jan, and Yuh Nung Jan. "Tiling of the Drosophila epidermis by multidendritic sensory neurons." Development 129, no. 12 (2002): 2867–78. http://dx.doi.org/10.1242/dev.129.12.2867.

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Insect dendritic arborization (da) neurons provide an opportunity to examine how diverse dendrite morphologies and dendritic territories are established during development. We have examined the morphologies of Drosophila da neurons by using the MARCM (mosaic analysis with a repressible cell marker) system. We show that each of the 15 neurons per abdominal hemisegment spread dendrites to characteristic regions of the epidermis. We place these neurons into four distinct morphological classes distinguished primarily by their dendrite branching complexities. Some class assignments correlate with known proneural gene requirements as well as with central axonal projections. Our data indicate that cells within two morphological classes partition the body wall into distinct, non-overlapping territorial domains and thus are organized as separate tiled sensory systems. The dendritic domains of cells in different classes, by contrast, can overlap extensively. We have examined the cell-autonomous roles of starry night (stan) (also known as flamingo (fmi)) and sequoia (seq) in tiling. Neurons with these genes mutated generally terminate their dendritic fields at normal locations at the lateral margin and segment border, where they meet or approach the like dendrites of adjacent neurons. However, stan mutant neurons occasionally send sparsely branched processes beyond these territories that could potentially mix with adjacent like dendrites. Together, our data suggest that widespread tiling of the larval body wall involves interactions between growing dendritic processes and as yet unidentified signals that allow avoidance by like dendrites.
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Geisler, Hildegard C., Jos IJkema-Paassen, Johan Westerga, and Albert Gramsbergen. "Vestibular Deprivation and the Development of Dendrite Bundles in the Rat." Neural Plasticity 7, no. 3 (2000): 193–203. http://dx.doi.org/10.1155/np.2000.193.

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Motoneuronal pools of muscles that subserve postural tasks contain dendrite bundles. We investigated in the rat the development of these bundles in the pools of the long back muscles and related this to postural development. Motoneurons and their dendrites were retrogradely labeled by injecting unconjugated cholera toxin subunit B (CTB) into the muscles of 54 normal rats from birth until adulthood and into 18 rats that were vestibularly deprived from the 5th postnatal day (P5). Dendrite bundles coursing in a transverse direction already occurred at P1. From P4, the first longitudinal bundles could be observed, but the major spurt in development occurred between P6 and P9, when conspicuous bundles developed coursing in rostro-caudal and tranverse directions. This is the age when rats become able to stand freely and walk a few steps. Around P20, the dendrite bundles attained their adult characteristics. Vestibular deprivation by plugging both semicircular horizontal canals did not lead to a retarded development of dendrite bundles nor to a changed morphology. This finding is remarkable, as behavioral analysis showed a delay in postural development by about 3 days. We hypothesize that dendrite bundles in the pools of the long back muscles function to synchronize the motoneurons in different spinal cord segments.
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Dissertations / Theses on the topic "Dendrite development"

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Le, Roux Peter David. "Neuron-glial interactions in dendrite growth." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27039.

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Interactions between neurons and glia occupy a central role in many aspects of development, maintenance, and function of the central nervous system (CNS). A fundamental event in CNS development is the elaboration of two distinct neuronal processes, axons and dendrites. The overall aim of this research was to characterize the interactions between central nervous system neurons and astroglial cells that regulate dendrite growth from cerebral cortical neurons. Embryonic (E18) mouse cerebral cortical neurons were cocultured with early postnatal (P4) rat astroglia derived from cerebral cortex, retina, olfactory bulb, mesencephalon, striatum and spinal cord. Axon and dendrite outgrowth from isolated neurons was quantified using morphological and double-labeling immunohistochemical techniques at 18 hours and 1, 3 and 5 days in vitro. Neurons initially extended the same number of neurites, regardless of the source of glial monolayer; however, astroglial cells differed in their ability to maintain primary dendrites. Homotypic cortical astroglia maintained the greatest number of primary dendrites. Astroglia derived from the olfactory bulb and retina maintained intermediate numbers of dendrites, whereas only a small number of primary dendrites were maintained by astroglia derived from striatum, spinal cord or mesencephalon. Initially longer axons were observed from neurons grown on astroglia that did not maintain dendrite number. After 5 days in vitro, axon growth was similar on the various monolayers, total primary dendrite outgrowth, however, was nearly threefold greater on astroglia derived from the cortex, retina and olfactory bulb than on astroglia derived from mesencephalon, striatum or spinal cord. This effect was principally on the number of primary dendrites rather than the elongation of individual dendrites and was independent of neuron survival. Similar morphological differences were observed after 5 days in vitro when cortical neurons were grown on polylysine in either a noncontact coculture system where astroglia continuously conditioned the culture medium or in astroglial conditioned medium. Preliminary biochemical analysis of the medium conditioned by cortical astroglia using heat and trypsin degradation, ultracentrifugation, dialysis, and heparin affinity chromatography suggested that a heparin binding protein with a molecular weight between 10 and 100kDa may be responsible for astroglial mediated dendrite growth. Neurons that were grown in medium conditioned by either mesencephalic or cortical astroglia for the first 24 hours followed by culture medium from astroglia of the alternate source for 4 days in vitro, confirmed that astroglia maintained, rather than initiated, the outgrowth of the primary dendritic arbor. In the next series of experiments, E18 mouse cortical neurons were cocultured with neonatal (P4) or mature (P12) rat astroglia derived from cortex and mesencephalon or astroglia derived from P4 and P12 lesioned cortex. After 5 days in vitro, the maturational age of astroglia did not appear to alter the extent of primary dendrite growth; instead dendrite growth reflected the region of the CNS from which the astroglia were derived. By contrast, a reduced ability to support axon growth from mouse cortical neurons in culture was observed on astroglia derived from mature rat cortex or mesencephalon. Reactive astroglia demonstrated similar neurite supporting characteristics to mature astroglia and were able to maintain dendrite growth, principally primary dendrite number. Axon elongation, however, was reduced on both neonatal and mature reactive astroglia. Neuron survival did not correlate with the ability of the various astroglia to support process outgrowth. Collectively these results indicate: 1) neuron-glial interactions are critical for the regulation of process outgrowth from embryonic cortical neurons in vitro, 2) axon and dendrite growth appear to be differently controlled by astroglia, 3) CNS astroglia demonstrate regional differences in maintaining, but not initiating growth of the primary dendritic arbor, 4) this effect may be due, in part, to release of a diffusible heparin binding protein factor, and 5) mature and reactive astroglia support primary dendrite, but limited axon growth. We propose therefore that the local astroglial environment maintains primary dendrite growth from neurons until synaptic contacts can be established. A mechanism that maintains the primary dendritic arbor and allows separate regulation of axon and dendrite growth, prior to the arrival of afferents, may be critical for establishing appropriate and specific synaptic connections. These findings have important implications in understanding development and function of the mammalian central nervous system and may lead to novel strategies for intervention in acute and chronic neurological disorders.
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Zhang, Ye. "The role of the secretory pathway in dendrite and axon development." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3390087.

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Krol, Alexandra. "Regulation of Neuronal Dendrite Development and Migration by the Atypical Cadherin Fat3." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467479.

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Neuronal shape and position are critical to the formation and function of neuronal circuits. Although neurons develop axons and dendrites cell-autonomously in vitro, how extracellular cues in vivo direct neurite specification and placement remains poorly understood. The role of atypical cadherin Fat3 in amacrine cell development illustrates how the same extracellular cue can guide both dendrite formation and migration. In the mouse retina, amacrine cells have a bipolar morphology during their migration. Upon reaching the nascent inner plexiform layer (IPL), they elaborate one neurite into the IPL and retract the other. Loss of Fat3 leads amacrine cells to develop an extra dendrite outside the IPL as well as errors in migration. We found Fat3 protein is concentrated at the IPL throughout amacrine cell development, suggesting Fat3 detects a directional signal. Here we investigated the signaling pathways upstream and downstream of Fat3 that mediate its role in amacrine cell development. In Drosophila, Fat’s ligand is Dachsous. Fat and Dachsous binding is modulated by the kinase Four-jointed. Our analysis of mutant retinas determined that Fat3 and vertebrate Four-jointed genetically interacted. However knockout studies of vertebrate Dachsous homologues suggested they are not relevant Fat3 ligands in the retina. Instead, analysis of retinas missing retinal ganglion cells suggested Fat3-mediated homophilic adhesion between amacrine cells may be important. Sparse loss of Fat3 from amacrine cells also led to extraneous neurites, suggesting Fat3 acts cell autonomously. Ex vivo live imaging revealed both migration and neurite dynamics were less directed in Fat3 mutant amacrine cells. We hypothesized Fat3 acts to target asymmetric localization of cytoskeletal regulators to the leading neurite. To identify downstream Fat3 effectors, we performed a pulldown assay using the Fat3 intracellular domain. We identified several cytoskeletal regulators as candidate binding partners. We focused on the actin regulators Ena/VASP and demonstrated a direct interaction with the Fat3 intracellular domain. In the retina, Ena/VASP localized with Fat3 to the IPL, and loss of Fat3 changed Ena/VASP distribution. Furthermore, forcing uniform membrane recruitment of Ena/VASP in developing amacrine cells phenocopied loss of Fat3. Together these results suggest Fat3 polarizes the activity of cytoskeletal effectors to help direct amacrine cell migration and dendrite placement.<br>Medical Sciences
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Mahnke, Amanda Hope. "Alterations to Dendrite Morphology in Response to Antipsychotic Drug Treatment and Hypoglutamatergia." Thesis, Tulane University School of Science and Engineering, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3639160.

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<p> Schizophrenia is a prevalent neurological disorder characterized by disrupted neuronal circuitry. Antipsychotic drugs (APDs) are capable of ameliorating the symptoms of schizophrenia with varying efficacy. Clozapine, the "gold-standard" for antipsychotic drug treatment, has been shown by this lab to induce the outgrowth of mediodorsal thalamic (MDT) dendritic arbor in rodents, a brain region which has altered function and decreased regional volume in schizophrenic patients. These studies further explored the ability of APD treatment to restructure dendrite arbor and the mechanisms of clozapine's ability to elaborate MDT arbor. Additionally, glutamate hypofunction is thought to contribute to the schizophrenic disease state. Using a novel model of perinatal glutamate hypofunction, we examined the long-term effects on dendritic architecture of developmental glutamate signaling disruption. </p><p> MDT dysfunction is hypothesized to contribute to cognitive symptoms of schizophrenia. Clozapine has increased efficacy in ameliorating these symptoms. To further understand clozapine's actions to remodel MDT dendritic architecture, we examined whether clozapine-induced morphological alterations are limited to the thalamus or if they also occur in additional regions associated with cognitive schizophrenic pathology, the hippocampus and striatum. We found that clozapine can induce dendritic remodeling in the hippocampus, but the not to the amplitude of remodeling seen in the thalamus, indicating that the MDT is uniquely altered by clozapine treatment and may be an important locus of clozapine's action. </p><p> The mechanisms of clozapine's remodeling of MDT arbor, we examined changes to mRNA and miRNA expression and calcium dynamics in the MDT in response to APD treatment. Clozapine-treatment altered the expression of genes involved in cytoskeletal remodeling, external membrane receptors, and calcium dynamics, as well as increased the rate of calcium influx into thalamic neurons. </p><p> Disruption to glutamate signaling has been hypothesized to contribute to schizophrenic pathology. Disruption to perinatal vesicular glutamate packaging along the corticolimbic axis has long term effects for neuronal morphology and function. Interestingly, we find that disruption along the corticolimbic axis also has downstream effects on MDT dendritic architecture. </p><p> These studies show that the MDT is an important locus of action for clozapine and is capable of remodeling dendritic architecture in response to afferent circuitry dysfunction.</p>
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Carlsen, Robert Means III. "Neural Plasticity and the Development of Intersensory Functioning in Bobwhite Quail (Colinus virginianus)." Diss., Virginia Tech, 1999. http://hdl.handle.net/10919/30196.

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Previous research has demonstrated that augmented prenatal sensory stimulation can influence the emergence of normal or species-typical patterns of intersensory perception. For example, unusually early visual experience can produce a facilitative effect on subsequent postnatal perceptual responsiveness, while substantially augmented prenatal visual stimulation can interfere with early postnatal responsiveness. In constructing a link between early experience and neuronal plasticity, it has been established that unusual visual experience can produce measurable changes in post-synaptic structures, particularly dendritic morphology, in brain areas responsible for vision. In avian species, the brain area responsible for vision is the visual Wulst, thought to be analogous to the mammalian visual cortex. This study examined the effects of differing amounts of augmented prenatal visual stimulation on the plasticity of neurons in the visual Wulst and on subsequent postnatal visual responsiveness to maternal cues in bobwhite quail chicks. Results revealed that the pattern of neuronal organization and postnatal behavior was influenced by the amount of prenatal visual experience subjects were provided. Specifically, chicks exposed to 240 min of prenatal visual stimulation during the last 24 hr prior to hatching had neurons with significantly fewer spines/10 mm dendrite and displayed accelerated patterns of species-typical visual responsiveness. In contrast, chicks provided 900 min of prenatal visual stimulation had more complex neurons (including more spines, longer dendrites, and more branches) and failed to display normal species-specific visual responsiveness in the days following hatching. These results suggest that neuronal organization in the bobwhite Wulst proceeds in a selective fashion, molded by experience, and appears to influence early perceptual development and organization during the perinatal period<br>Ph. D.
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Gaddy, Joshua L., and Joshua L. Gaddy. "The Effects of Developmental Nicotine Exposure on Hypoglossal Motoneuron Primary Dendrite and Soma Development in the Neonatal Rat." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/621005.

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Nicotine from smoking or from other products containing nicotine has adverse effects on the fetus during pregnancy, such as respiratory problems. Our laboratory has previously shown that exposure to nicotine during development (DNE) alters hypoglossal motor neuron (XII MN) function, including decreased excitatory synaptic input, desensitized nicotinic acetylcholine receptors, increased input resistance, and differences in the precision and reliability of spike timing in XIIMNs. Evidence of DNE effects on XIIMN function prompted us to test the hypothesis that DNE will affect the development of primary dendrites and the soma. Brainstem slices were collected from neonates and motoneurons were filled with neurobiotin via whole-cell patch clamp. Filled cells were visualized with heavy metal intensified-3,3'-Diaminobenzidine (DAB) reaction. DAB-stained cells were analyzed using Neurolucida hardware and software. On average, the maximum soma diameter of more rostral XIIMNs was larger than that in more caudal cells. Also, caudal XIIMNs had more primary nodes than rostral XIIMNs, and there was a significant treatment effect on minimum soma diameter (Control, 13.76 ± 0.71 µm; DNE, 18.09 ± 1.22 µm). The results from this study uncovered potential effects of nicotine on XIIMNs found in rostral and caudal regions of the hypoglossal nucleus.
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Sears, James Cooper. "FoxO Regulates Microtubule Dynamics and Polarity to Promote Dendrite Branching in Drosophila Sensory Neurons." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1476705366788041.

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Molumby, Michael Jacob. "Gamma-protocadherin Cis- and Trans-interactions regulate the development of dendrite arbors and synapses in the cerebral cortex." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5815.

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The alpha-, beta-, and gamma-Protocadherins (gamma-Pcdhs) are cadherin superfamily adhesion molecules encoded by clustered gene families. The 22 gamma-Pcdhs are combinatorially expressed in the central nervous system (CNS) by neurons and astrocytes, and play critical roles in synaptogenesis, dendrite arborization, and the survival of subsets of neurons. The gamma-Pcdhs promiscuously form cis-multimers that interact strictly homophilically in trans (Molumby et al., 2016; Schreiner and Weiner, 2010); the alpha- and beta-Pcdhs were subsequently shown to interact in a similar homophilic manner (Rubinstein et al., 2015; Thu et al., 2014). The Pcdh gene clusters thus have the potential to generate millions of distinct adhesive interfaces, providing CNS cells with molecular identities that shape neuronal morphology. We demonstrated previously that, in mice lacking the gamma-Pcdhs in the cerebral cortex, pyramidal neurons exhibit severely reduced dendrite arborization (Garrett et al., 2012a). This, combined with many studies of gamma-Pcdh interactions in vitro, suggests that homophilic, adhesive gamma-Pcdh interactions between neurons, and between neurons and glia, provide a positive signal for dendrite growth. However, in retinal starburst amacrine cells and cerebellar Purkinje cells, loss of the gamma-Pcdhs resulted in aberrant dendrite fasciculation and self-crossing (Lefebvre et al., 2012), suggesting that these molecules can mediate repulsive self-avoidance between a neuron’s own dendrites. In Chapter I of this thesis I utilized transgenic mice to manipulate expression in vivo, to show that the complexity of a cortical neuron’s dendritic arbor is determined by homophilic gamma-Pcdh isoform matching with other cells. Expression of the same single isoform in a neuron can result in either exuberant, or minimal, dendrite complexity depending on whether surrounding cells express the same isoform. Additionally, loss of gamma-Pcdh in astrocytes, or induced astrocyte-neuron mis-matching, reduces dendrite complexity cell non-autonomously. This indicates a neuron’s pattern of connectivity is indeed regulated by specific interactions between cells that are distinct from the repulsive self-avoidance seen in isoneuronal processes of planar cell types. In addition to modulating dendrite branch development, the gamma-Pcdhs have been shown to regulate the progression of spinal cord synaptogenesis (Garrett and Weiner, 2009). A role for these molecules in cortical dendritic spines and synapses, however, had yet not been examined. In Chapter II of this thesis, I provide evidence that the gamma-Pcdhs negatively regulate synapse formation and spine morphogenesis in forebrain neurons. Mice lacking all gamma-Pcdhs in the cortex exhibit significantly increased spine and synapse density in vivo, while spine density is significantly decreased in mice overexpressing one of the 22 gamma-Pcdh isoforms. To explain this functional result, we present in vitro evidence to show that gamma-Pcdhs physically and functionally interact with the synaptic cell adhesion molecule neuroligin-1. This work suggests a potential new mechanism by which gamma-Pcdhs regulate the “choice” between dendrite arbor growth and formation and/or stabilization of dendritic spines and synapses in the developing brain. Given that disruptions in the pattern and density of dendritic arbors and spines are a hallmark of neurodevelopmental disorders such as autism and Down, Rett, and fragile X syndromes, my work may provide the basic science foundation for future therapeutic approaches focused on Pcdhs and their associated signaling pathways.
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9

Dimitrova, Svetla. "Physiological Roles of Robo Receptor during dendrite development of the multidendritic arborization neurons of the Drosophila peripheral nervous system." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-78347.

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Amini, Mandana. "Analysis of Conditional Knock-out of Calpain Small Subunit, capns1, in Central Nervous System Development and Function." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31360.

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Calpains, a highly conserved family of calcium-dependent cysteine proteases, are divided in two groups; classical and non-conventional calpains. Calpain-1 and calpain-2, the classical ones, are ubiquitously expressed and abundant in the CNS. Findings through different experimental approaches, predominantly pharmacological calpain inhibitors, proposed the necessity of the proteases for the modulation of various biological events particularly in the CNS, or a functional link between calpain and neurodegeneration. Significant functions associated with calpain activity are neuronal proliferation/differentiation, signal transduction, apoptosis, and synaptic plasticity; or neuronal death in Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and ischemic stroke. However, due to limited insights of the approaches taken, such as non-specificity of the inhibitors, the exact roles of calpains in the CNS and the key mechanisms underlying them remain controversial. Calpain-1/calpain-2 germline knock-out are embryonic lethal at a very early stage hindering the use of these lines as mouse models for CNS studies. Accordingly, this thesis research introduced a unique brain-specific calpain-1/calpain-2 knock-out and explored the role of the proteases in brain development/function and in neuronal death. The first set of analyses examined how the elimination of calpain-1/calpain-2 activities in mouse brain impacts CNS development in general and synaptic plasticity in CA1 neurons of hippocampus. CNS-specific elimination of CAPNS1, the common small subunit, abolished calpain-1/calpain-2 activities in mouse brain. In contrast to Calpain-1/calpain-2 germ line knock-outs, the brain-specific knock-outs are viable and the general development of mouse brain is normal. However, morphology of dendrites in pyramidal neurons of the hippocampal CA1 region showed significantly decreased dendritic branching complexity and spine density. Consistent with dendrite morphological abnormalities, electrophysiological analyses revealed a significant decrease in field excitatory postsynaptic potentials, long term potentiation, and learning and memory in the hippocampal CA1 neurons of the mutants. In the second part of this research we investigated the direct role of the calpains in neuronal death and their potential downstream targets in in vitro models of PD and ischemic stroke. Our findings indicated that ablation of calpains activity improves survival of different types of neurons against mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+), glutamate, and hypoxia. Importantly, we demonstrated an increase in p35-cleavage to p25, a cyclin dependent kinase 5 (Cdk5) activator, and that restoration of p25 significantly suppresses the neuronal survival associated with calpain deficiency. Taken together, this work unequivocally establishes two central roles of calpain-1/calpain-2 in CNS function in plasticity and neuronal death.
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Books on the topic "Dendrite development"

1

Levinson, Laurie H. Flight software development for the Isothermal Dendritic Growth Experiment. National Aeronautics and Space Administration, 1990.

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Levinson, Laurie H. Flight software development for the Isothermal Dendritic Growth Experiment. National Aeronautics and Space Administration, 1990.

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Bohnenkamp, Hermann Richard. Bioprocess development for the generation of monocycte-derived dendritic cells: Applicability in breast cancer immunotherapy. Forschungszentrum Jülich GmbH, Institut für Biotechnologie, 2004.

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Kapfhammer, Josef P. Cellular and molecular control of dendritic growth and development of cerebellar Purkinje cells. Elsevier, 2004.

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Voorbij, H. A. M. Dendritic cells and the development of thyroid autoimmune disease and type 1 diabetes mellitus. Thesis, 1989.

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Huang, Eric, Kazuo Emoto, Rachel Wong, and Casper Hoogenraad. Dendrites: Development and Disease. Springer, 2018.

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Tate, Marcia L. Shouting - Won't Grow Dendrites: A Multimedia Kit for Professional Development. Corwin Press, 2008.

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Advanced dendritic web growth development and development of single-crystal silicon dendritic ribbon and high-efficiency solar cell program: Final report. Westinghouse R&D Center, 1986.

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Stashwick, Caitlin, Brian J. Czerniecki, and Janos L. Tanyi. Dendritic Cell Vaccine Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0008.

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Dendritic cell vaccine therapy has emerged as an exciting new field in immunotherapy in ovarian cancer over the past two decades. This chapter reviews the biology of dendritic cells, including dendritic cell subsets, development, activation, and maturation as well as strategies for clinical use of dendritic cell vaccines. While there is encouraging data in preclinical work for dendritic cell vaccine, the outcomes of clinical trials have not shown robust responses. A summary of the clinical trials using dendritic cell vaccines in ovarian cancer is reviewed. Treatment-related toxicities and potential therapies to increase clinical efficacy are also discussed.
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Reading And Language Arts Worksheets Dont Grow Dendrites A Multimedia Kit For Professional Development. Corwin Press, 2010.

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Book chapters on the topic "Dendrite development"

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Walrath, Robert. "Dendrite." In Encyclopedia of Child Behavior and Development. Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_798.

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Cline, Hollis T. "Experience-Dependent Dendritic Arbor Development." In Dendrites. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56050-0_13.

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Cheung, Zelda H., and Nancy Y. Ip. "Cdk5 in Dendrite and Synapse Development: Emerging Role as a Modulator of Receptor Tyrosine Kinase Signaling." In Cyclin Dependent Kinase 5 (Cdk5). Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_5.

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D’Orazi, Florence D., and Takeshi Yoshimatsu. "Development of Synaptic Input Patterns on Dendrites of Retinal Neurons." In Dendrites. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56050-0_19.

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Scheibel, Arnold B. "Dendritic Structure and Language Development." In Developmental Neurocognition: Speech and Face Processing in the First Year of Life. Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-015-8234-6_5.

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Steinman, Ralph M., Maggie Pack, and Kayo Inaba. "Dendritic Cell Development and Maturation." In Advances in Experimental Medicine and Biology. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_1.

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Jacobson, Marcus. "Formation of Dendrites and Development of Synaptic Connections." In Developmental Neurobiology. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-4954-0_6.

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Oliveira, Joaquim M., João F. Mano, and Rui L. Reis. "Progress in Dendrimer-Based Nanocarriers." In Biomimetic Approaches for Biomaterials Development. Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527652273.ch19.

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Freeman, A. W., and J. M. J. Fréchet. "Developments in the Accelerated Convergent Synthesis of Dendrimers." In Dendrimers and Other Dendritic Polymers. John Wiley & Sons, Ltd, 2002. http://dx.doi.org/10.1002/0470845821.ch4.

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Perrin, Dominique. "Groups, Languages and Dendric Shifts." In Developments in Language Theory. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98654-8_5.

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Conference papers on the topic "Dendrite development"

1

Nayak, Saurav K., Sanjay K. Mishra, Christ P. Paul, Arackal N. Jinoop, Sunil Yadav, and Kushvinder S. Bindra. "Effect of Laser Energy Density on Bulk Properties of SS 316L Structures Built by Laser Additive Manufacturing Using Powder Bed Fusion." In ASME 2019 Gas Turbine India Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/gtindia2019-2452.

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Abstract Laser Additive Manufacturing using Powder Bed Fusion (LAM-PBF) is one of the revolutionary technologies playing a key role in fourth industrial revolution for redefining manufacturing from mass production to mass customization. To upkeep the pace, Raja Ramanna Centre for Advanced Technology (RRCAT) has indigenously developed an LAM-PBF system and it is being used for process and component development for various engineering applications. This paper reports a parametric investigation to evaluate the influence of process parameters on the sample properties and to develop the process window for fabricating complex shaped engineering components. In the present work, an experimental investigation is carried out to investigate the effect of Laser Energy density (LED) on the porosity, microstructure and mechanical properties of SS 316L bulk structures fabricated by LAM-PBF system. LED is a combined parameter simultaneously considering the effect of Laser Power (P), Scan Speed (v), hatch spacing (h) and layer thickness (t). The effect of three LED values such as 83.33 J/mm3, 253.97 J/mm3 and 476.19 J/mm3 is investigated in the present work by building cuboidal samples at a layer thickness of 75 microns. Porosity is estimated using area fraction method in optical microscopy and it is found that the minimum porosity of 0.14 % and pore area of 1.28 mm2 are observed at 253.97 J/mm3. Maximum porosity of 18.85 % is observed at 83 J/mm3 due to incomplete fusion defects. However, porosity observed at 475 J/mm3 is 6.56 % with average pore size of 17.8 mm2. Microstructural studies show primarily columnar growth in all the samples with fine dendrites. The dendrite size is observed to be 3.2 μm, 2.4 μm and 1.46 μm at 83.33 J/mm3, 253.97 J/mm3 and 476.19 J/mm3 respectively. Micro-hardness and single cycle automatic ball indentation studies are found to be in agreement with dendritic size, with lower hardness at larger dendrite size. X-Ray Diffraction (XRD) studies indicate similar peaks at all the conditions, with slight peak shift observed with increase in LED primarily due to higher amount of residual stress. Thus, it can be inferred that LED of 253.97 J/mm3 is suitable for fabricating engineering components due to combination of lower porosity and fine dendritic structure.
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Hu, Xuefei, John W. Sutherland, and James M. Boileau. "Characterizing the Effect of 319 Aluminum Microstructure on Machinability: Part 1 — Model Development." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-79653.

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This two-part paper is directed at the development of a machining force model that addresses key microstructural features of 319 Aluminum. In Part 1 of this paper, a machining force model is presented that incorporates microstructural effects. Secondary Dendrite Arm Spacing (SDAS) is identified as a significant microstructure feature of 319 aluminum in terms of machinability, and the SDAS is related to the solidification rate. A new material constitutive relationship that incorporates SDAS microstructure effects is proposed. In Part 2 of this paper, the results from material tests and machining experiments are presented. A new methodology for estimating parameters within the material constitutive model is described, and force model predictions are compared with the results from machining tests. The comparison reveals an excellent agreement between measured and predicted forces.
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Nakagawa, K., T. Takaki, Y. Morita, and E. Nakamachi. "2D Phase-Field Analyses of Axonal Extension of Nerve Cell." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64281.

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In this study, we aimed to develop a computer-aided simulation technique to predict the axonal extension in the neuronal network evolution processes for design new scaffolds to activate the nerve cell and promote the nerve regeneration. We developed a mathematical model of axonal extension by using phase-field method and evaluated the validity of the mathematical model by comparison with the experiments. In the previous experimental studies, the peripheral nerve scaffold has been introduced to guide the axonal extension. Damaged part of nerve was replaced by the artificial tube as the scaffold to induce the axonal growth through the artificial tube and regenerate the nerve network. However, the scaffold made of biodegradable materials has a problem that it is degraded and absorbed before the nerve regenerate, and then the nerve cannot regenerate. Therefore, there is a need for the design and development of a scaffold for nerve regeneration to promote nerve regeneration. For that purpose, it is necessary to understand the difference between the axonal extensions by the surrounding environment, such as the shape or materials of the scaffold for nerve regeneration. In particular, the numerical technique to analyze the remodeling process of the nerve in the scaffold is strongly required to be established because the in-vivo experimental observation technology at the micro scale, bioethical issues in the animal experiment and requires time and money are also remained as unresolved problems. In this study, we developed a new simulation code which employed the phase-field method to predict the two-dimensional dendritic and axonal growth processes of nerve cells on cultivation scaffolds. We curried out the phase-field analyses to make clear how the parameters of Kobayashi–Warren–Carter (KWC) phase-field model affected on the morphologic growths of dendrite and axon. Simultaneously, we had observed the axonal extension process by using the PC-12D cells with nerve growth factor (NGF) on two-dimensional cultivation dish. Based on these axonal extension observation results, we approximated the morphological changes and establish the phenomenological model for phase-field analysis. Finally, we confirmed the validity of our newly developed phase-field simulation scheme in two dimensions by comparison with the experiments.
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Guo, Taiming, Hongmin Li, and G. X. Wang. "Development of Irregular Interface Morphology During Unidirectional Solidification of Succinonitrile." In ASME 2003 Heat Transfer Summer Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/ht2003-47215.

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This paper reports an experimental investigation on irregular interface morphology patterns developed in thin-film unidirectional solidification of pure succinonitrile. Solidification experiments have been conducted under various temperature gradients and interface velocities. Several irregular patterns have been observed including titled dendrites, degenerate dendrites, and seaweed. It is found that as the temperature gradient increases, steady titled dendrites may evolve into degenerate dendrites and eventually to seaweed. With the same grain orientation, the irregular patterns may transform from one form to another as the growth condition changes. Observations demonstrate that normal dendrites exhibit a higher growth rate than seaweed pattern and would overgrow them. Irregular pattern may also become strongly dynamic and different patterns may evolve into each other during growth within the same experiment. These results should shed a light into the understanding of the interface morphology development during solidification.
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Felicelli, Sergio D., and David R. Poirier. "Modeling of Solidification and Filling of Thin-Section Castings." In ASME 2005 Summer Heat Transfer Conference collocated with the ASME 2005 Pacific Rim Technical Conference and Exhibition on Integration and Packaging of MEMS, NEMS, and Electronic Systems. ASMEDC, 2005. http://dx.doi.org/10.1115/ht2005-72682.

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A finite element model for simulating dendritic solidification of multicomponent-alloy castings is used to study the filling and solidification of castings of thin cross section. The model solves the conservation equations of mass, momentum, energy, and alloy components and couples the solution with the thermodynamic of the multicomponent alloy through a phase diagram equation. The transport of mass and energy in the mushy zone is done considering the mushy zone as a porous medium of variable porosity. The same set of conservations equations are used for the liquid, solid and mushy zones, in which the volume fraction of liquid acts as the variable that makes the equations transition continuously from one zone to another (Felicelli et al. [1]). During filling, the model tracks the advancing front as the metal flows into the thin mold, and solidification is calculated as the metal loses energy by convection and radiation to the mold, including the dynamic calculation of view factors. The code supports two fluid models that emulate the flow behavior under equiaxed or columnar solidification. In the former case a slurry fluid model is used in which the viscosity is determined by the volume fraction of solid. In this slurry state, the solid and liquid move at the same velocity. For the case of columnar solidification, the solid is fixed and the liquid flows through a porous structure of dendrictic solid. The model development is based on the work by Felicelli et al. [2], to which several features were added, including a front-tracking technique (Gao [3]) and thermal radiation boundary conditions. Calculations for Ni and Al alloys were performed to illustrate the effect of several physical and operation parameters in the filling of a horizontal channel of thin thickness. A wide range of process parameters was tested in order to determine how much of the channel length could be filled before blockage of flow by solidification occurred. In a separate section, the effect of alloy concentration on the fluidity was studied using a Pb-Sn hypoeutectic system, and the importance that the dendrite breaking phenomenon can have on the results is shown. Conclusions about the parameters that most influence the filling process are presented, as well as recommendations on which experimental data are more critical in order to conduct a proper validation of this type of models.
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LEVINSON, LAURIE, EDWARD WINSA, and M. GLICKSMAN. "Flight software development for the isothermal dendritic growth experiment." In 28th Aerospace Sciences Meeting. American Institute of Aeronautics and Astronautics, 1990. http://dx.doi.org/10.2514/6.1990-744.

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Huang, R., H. Tawfik, and A. K. Nagar. "Artificial Dendritic Cells Algorithm for Online Break-In Fraud Detection." In 2009 Second International Conference on Developments in eSystems Engineering (DESE). IEEE, 2009. http://dx.doi.org/10.1109/dese.2009.59.

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Lu, Shuhua, Xiang Ling, and Jinchun Zhang. "Investigation of Preparation Processes and Corrosion Resistance of NiCrBSi Coatings Fabricated by Laser-High Frequency Induction Hybrid Cladding." In ASME 2016 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/pvp2016-63109.

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The surface of many key components used in petrochemical industry may be damaged by corrosion, wear and overheat during service. This damage can make a significant impact on the safe and reliable operation process of the device. Low alloy steel is widely used to manufacture pressure vessels and pipes because of the higher strength and good processing properties, but has poor corrosion resistance and wear resistance. Laser cladding is an advanced and effective surface modification technology. It can improve the surface properties of the matrix material at lower cost. But these claddings crack easily due to the high temperature gradient in the laser molten pool and physical properties differences between the cladding material and matrix. This problem has affected the development of laser cladding. Laser-high frequency induction hybrid cladding is a novel technology which combines laser beam heat source and induction power. It can decrease the cracks in the claddings effectively and has been received significant attentions in recent years. Nickel base alloy powders have good corrosion resistance, wettability and high temperature lubricity. In this research, NiCrBSi composite claddings were fabricated on the surface of low alloy steel by the way of laser-high frequency induction hybrid cladding and coaxial powder feeding. The optimum cladding technology parameters to obtain the cladding layers that with good metallurgical combination, reasonable dilution rate and without cracks and defects were developed by optimizing the processing parameters such as laser power, powder feeding rate, laser scanning speed and induction heating temperature. The hardness distribution, microstructure, element distribution and phase of the cladding layers fabricated by the optimum parameters were systematically investigated by means of micro-hardness tester, optical microscopy (OM). Compared with the untreated material, experiment results show that the micro-hardness from substrate to NiCrBSi cladding layer exhibits step distribution, and the hardness of the NiCrBSi cladding layer is higher than that of the base metal. The microstructure showed good metallurgical bonding between NiCrBSi cladding and substrate had been achieved. In addition, directionally solidified microstructures were deposited. From the top to bottom of the cladding layer, the microstructures are, in order, equiaxed crystal, dendrite crystal, cellular crystal, columnar crystal and plane crystals. The corrosion resistance of the base metal and specimens manufactured by laser-high frequency induction hybrid cladding were evaluated in 3.5% NaCl solution by electrochemical testing. The experimental results demonstrate that the corrosion resistance of the NiCrBSi cladding layer fabricated by laser-high frequency induction hybrid cladding technology is better than the base metal.
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Babushkina, Nina. "Simplest Mathematical Model of Anti-Tumor Therapy Based on Dendritic Cells." In 2020 13th International Conference Management of large-scale system development (MLSD). IEEE, 2020. http://dx.doi.org/10.1109/mlsd49919.2020.9247754.

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Paringer, R. A., and A. V. Kupriyanov. "Development of parallel implementation for the dendritic crystallograms modeling algorithm." In Information Technology and Nanotechnology-2015. Image Processing Systems Institute, Russian Academy of Sciences, Samara, Russia, Samara State Aerospace University, Samara, Russia, 2015. http://dx.doi.org/10.18287/1613-0073-2015-1490-285-289.

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Reports on the topic "Dendrite development"

1

Dewhurst, Stephen. Dendritic Cell-Targeted Phage Vectors for Breast Cancer Vaccine Development. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada417050.

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Gong, Jianlin. Development of a Novel Vaccine with Fusions of Dendritic and Ovarian Cancer Cells from Patients. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada418726.

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Gong, Jianlin. Development of a Novel Vaccine with Fusions of Dendritic and Ovarian Cancer Cells from Patients. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada404671.

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