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Dissertations / Theses on the topic 'Neural development'
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De, Sousa C. A. Ferreira. "Vertebrate somite development and neural patterning." Thesis, Cranfield University, 2013. http://dspace.lib.cranfield.ac.uk/handle/1826/10567.
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The segmentation of the axial skeleton and peripheral nervous system involves a complex integration of multiple patterning molecules. For the latter, axon-repelling molecules in the posterior half-sclerotome are particularly important. This study built on a previously performed mouse microarray screen for novel candidate genes in the posterior half-sclerotome. Multiple candidates were selected for whole-mount in situ hybridization in chick. Two were expressed in the posterior half-sclerotome: thrombin receptor (F2R) and fibronectin leucine rich transmembrane protein-2 (Flrt2). Flrt2 was selected for siRNA-mediated knockdown and a new in ovo transfection technique for somites successfully developed. Scrambled siRNA-transfection did not affect morphogenesis, somite patterning or axon guidance. However, Flrt2 siRNA-transfection resulted in defects in notochord, dermomyotome and neural tube morphogenesis, and in the de-fasciculation and mis-targeting of spinal axons into the posterior half-sclerotome and dermomyotome. Hence, Flrt2 may be a chemorepellent for spinal axons. An unidentified peanut agglutinin (PNA)-binding glycoprotein in the posterior half-sclerotome was previously shown to repel spinal axons. In this project, the expression of a family of mucin-type O-glycosylation enzymes (which could glycosylate the PNA-binding protein) was investigated by whole-mount in situ hybridization in chick, but none was differentially expressed in the posterior half-sclerotome. One candidate for the PNA-binding glycoprotein, Presenilin1, was investigated because of previously published loss of spinal nerve segmentation in Presenilin1 mutants. However, analysis of Presenilin1-hypomorphic mutant mouse embryos showed this was not the PNA-binding molecule. Live-immunostaining for a second candidate, prolyl 4-hydroxylase, beta polypeptide (P4HB), showed its expression coincided with PNA-binding at the surface of posterior half-sclerotome cells. P4HB siRNA-transfection into somites reduced PNA binding and disrupted spinal axon segmentation and expression of a posterior sclerotome marker, Uncx4.1. Overall, these results suggest that P4HB is a strong candidate to be the key PNA-binding glycoprotein in the posterior half-sclerotome that repels spinal axons.
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Mayer, Eric. "Development of intrastriatal neural transplantation techniques." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282924.
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Fourla, Danai-Dionysia. "Retinoid signalling in Xenopus neural development." Thesis, University of Portsmouth, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439189.
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This thesis focuses on the use of animal caps to address questions concerning neural induction, patterning and neurogenesis in Xenopus embryos. Animal caps can be neuralised by the inhibition of BMPs through the action of inhibitors, such as noggin, but they do not form neurons. Instead, primary neurogenesis requires additional signalling by retinoic acid (RA), acting through the retinoid receptors, RARIRXR. In the presence of RA, retinoid signalling (RS) activates gene expression. Key target genes of RS during development are the Hox genes that are believed to be important for both posterior patterning and neurogenesis. In contrast, in the absence of RA, RS promotes active repression; a process that is required for normal head formation. However, much less is known of the genes that are affected by active repression. Although RS is sufficient to promote neurogenesis in noggin-neuralised animal caps, it is likely to be working in conjunction with other, endogenous, signalling pathways, mediated for example by FGF and Wnt. In this study, animal caps were analysed for signalling molecule expression after neuralisation by noggin and treatment with RARlRXR (±RA) and it was shown that the expression of some, but not all, FGFs and Wnts respond to RS in the animal cap. This may be significant for neural induction, patterning and neurogenesis; related processes in the animal cap. In addition, the receptor isotypes RARa and RARy seem to elicit different responses from some genes. Positive RS (RARlRXR+RA) was shown to promote posterior markers, such as Hox genes and the expression of Wnt3A. However, negative RS (RARlRXR-RA) was shown to inhibit Wnt3A and activate xSaiF. Consequently, RARs promote Wnt signalling posteriorly via positive signalling and inhibit Wnt signalling anteriorly by negative signalling. In conclusion, this thesis shows that animal caps can be used to investigate the effects of RS in Xenopus neural development and indicates a major role for RS along the length of the AlP axis of the embryo.
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Townsend, Joseph Paul. "Artificial development of neural-symbolic networks." Thesis, University of Exeter, 2014. http://hdl.handle.net/10871/15162.
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Artificial neural networks (ANNs) and logic programs have both been suggested as means of modelling human cognition. While ANNs are adaptable and relatively noise resistant, the information they represent is distributed across various neurons and is therefore difficult to interpret. On the contrary, symbolic systems such as logic programs are interpretable but less adaptable. Human cognition is performed in a network of biological neurons and yet is capable of representing symbols, and therefore an ideal model would combine the strengths of the two approaches. This is the goal of Neural-Symbolic Integration [4, 16, 21, 40], in which ANNs are used to produce interpretable, adaptable representations of logic programs and other symbolic models. One neural-symbolic model of reasoning is SHRUTI [89, 95], argued to exhibit biological plausibility in that it captures some aspects of real biological processes. SHRUTI's original developers also suggest that further biological plausibility can be ascribed to the fact that SHRUTI networks can be represented by a model of genetic development [96, 120]. The aims of this thesis are to support the claims of SHRUTI's developers by producing the first such genetic representation for SHRUTI networks and to explore biological plausibility further by investigating the evolvability of the proposed SHRUTI genome. The SHRUTI genome is developed and evolved using principles from Generative and Developmental Systems and Artificial Development [13, 105], in which genomes use indirect encoding to provide a set of instructions for the gradual development of the phenotype just as DNA does for biological organisms. This thesis presents genomes that develop SHRUTI representations of logical relations and episodic facts so that they are able to correctly answer questions on the knowledge they represent. The evolvability of the SHRUTI genomes is limited in that an evolutionary search was able to discover genomes for simple relational structures that did not include conjunction, but could not discover structures that enabled conjunctive relations or episodic facts to be learned. Experiments were performed to understand the SHRUTI fitness landscape and demonstrated that this landscape is unsuitable for navigation using an evolutionary search. Complex SHRUTI structures require that necessary substructures must be discovered in unison and not individually in order to yield a positive change in objective fitness that informs the evolutionary search of their discovery. The requirement for multiple substructures to be in place before fitness can be improved is probably owed to the localist representation of concepts and relations in SHRUTI. Therefore this thesis concludes by making a case for switching to more distributed representations as a possible means of improving evolvability in the future.
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Cottens, Pablo Eduardo Pereira de Araujo. "Development of an artificial neural network architecture using programmable logic." Universidade do Vale do Rio dos Sinos, 2016. http://www.repositorio.jesuita.org.br/handle/UNISINOS/5411.
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Normalmente Redes Neurais Artificiais (RNAs) necessitam estações de trabalho para o seu processamento, por causa da complexidade do sistema. Este tipo de arquitetura de processamento requer que instrumentos de campo estejam localizados na vizinhança da estação de trabalho, caso exista a necessidade de processamento em tempo real, ou que o dispositivo de campo possua como única tarefa a de coleta de dados para processamento futuro. Este projeto visa criar uma arquitetura em lógica programável para um neurônio genérico, no qual as RNAs podem fazer uso da natureza paralela de FPGAs para executar a aplicação de forma rápida. Este trabalho mostra que a utilização de lógica programável para a implementação de RNAs de baixa resolução de bits é viável e as redes neurais, devido à natureza paralelizável, se beneficiam pela implementação em hardware, podendo obter resultados de forma muito rápida.
Currently, modern Artificial Neural Networks (ANN), according to their complexity, require a workstation for processing all their input data. This type of processing architecture requires that the field device is located somewhere in the vicintity of a workstation, in case real-time processing is required, or that the field device at hand will have the sole task of collecting data for future processing, when field data is required. This project creates a generic neuron architecture in programmabl logic, where Artifical Neural Networks can use the parallel nature of FPGAs to execute applications in a fast manner, albeit not using the same resolution for its otputs. This work shows that the utilization of programmable logic for the implementation of low bit resolution ANNs is not only viable, but the neural network, due to its parallel nature, benefits greatly from the hardware implementation, giving fast and accurate results.
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Waldhuber, Markus. "Neural stem cells in development and cancer." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-92214.
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Subbarao, Tara. "Effects of nicotine on embryological neural development." Connect to resource, 2007. http://hdl.handle.net/1811/24616.
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Thesis (Honors)--Ohio State University, 2007.Title from first page of PDF file. Document formatted into pages: contains 18 p.; also includes graphics. Includes bibliographical references. Available online via Ohio State University's Knowledge Bank.
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Chuong, Amy (Amy S. ). "Development of next-generation optical neural silencers." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/69521.
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Thesis (S.M.)--Massachusetts Institute of Technology, School of Architecture and Planning, Program in Media Arts and Sciences, 2011.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 65-74).
The ability to rapidly and safely silence the electrical activity of individual neurons or neuron populations is invaluable in the study of brain circuit mapping. The expression of light-driven ion channels and pumps allows these pathways to be observed, mapped and controlled with millisecond timescale resolution. We here show that it is possible to mediate the powerful multiple-color silencing of neural activity through the heterologous expression of light-driven outward proton pumps and inward chloride pumps. We characterized a number of novel opsins through an exploration of ecological and genomic diversity, and further boosted opsin function and trafficking through the appendage of signal sequences. The green-light drivable archaerhodopsin-3 (Arch) from Halorubrum sodomense and the yellow-light drivable archaerhodopsin from Halorubrum strain TP009 (ArchT) are able to mediate complete neuron silencing in the in vivo awake mouse brain, and the blue-light drivable proton pump from Leptosphaeria maculans (Mac) opens up the potential for the multiple-color control of independent neuron populations. Finally, the principles outlined here can be extrapolated to the larger context of synthetic physiology.
by Amy Chuong.
S.M.
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Canales, Andrés. "Development of neural probes using thermal drawing." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111316.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Materials Science and Engineering, 2017.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 127-147).
The treatment of neurodegenerative and neurological conditions relies on better understanding the system that they afflict. However, the tools currently available to probe neural circuits are often limited to use in short-term studies primarily due to poor of biocompatibility. To address this challenge, flexible, minimally invasive neural probes were fabricated using a thermal drawing process, with polymers serving as their main structural constituent. Through the use of different polymers, probes containing arrays of tin electrodes as small as 5 [mu]m were fabricated, as were probes combining capabilities for electrical recording, optical stimulation, and drug delivery. A technique was developed to combine functionalities of these devices into a single probe to study the effect of optical stimulation with different waveforms on the brain activity. To break the longitudinal symmetry inherent to probes fabricated using the thermal drawing process, and to allow the incorporation of functionalities along the probe length, a method to combine thermal drawing with a method commonly used to fabricate neural probes, photolithography, was developed, along with the selection of the polymer that would allow consecutive processing using these two techniques. All of the fabricated probes were characterized and tested in vivo by implantation into mice and assessing their functionality. High signal-to-noise ratio (13±6) recordings were obtained using multielectrode arrays. Recordings of neural activity during simultaneous optical stimulation and drug delivery were performed with multifunctional probes. Hybrid probes combining metal electrodes with a polymer waveguide were used to study the response of large groups of neurons to different forms of optical stimuli. Most importantly, the biocompatibility of these probes was assessed over a 3 month period and compared favorably to that of steel microwires of similar size.
by Andrés Canales.
Ph. D.
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Biswas, Sayantanee. "Role of Protocadherins in Zebrafish Neural Development." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354720718.
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Westermann, Gert. "Constructivist neural network models of cognitive development." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22733.
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In this thesis I investigate the modelling of cognitive development with Constructivist neural networks. I argue that the constructivist nature of development, that is, the building of a cognitive system through active interactions with its environment, is an essential property of human development and should be considered in models of cognitive development. I evaluate this claim on the basis of evidence from cortical development, cognitive development, and learning theory. In an empirical evaluation of this claim, I then present a constructivist neural network model of the acquisition of the English past tense and of impaired inflectional processing in German agrammatic aphasics. The model displays a realistic course of acquisition, closely modelling the U-shaped learning curve and more detailed effects such as frequency and family effects. Further, the model develops double dissociations between regular and irregular verbs. I argue that the ability of the model to account for the human data is based on its constructivist nature, and this claim is backed by an analogous, but non-constructivist model that does not display many aspects of the human behaviour. Based on these results I develop a taxonomy for cognitive models that incorporates architectural and developmental aspects besides the traditional distinction between symbolic and subsymbolic processing. When the model is trained on the German participle and is then lesioned by removing connections, the breakdown in performance reflects the profiles of German aggrammatic aphasics. Irregular inflections are selectively impaired and are often overregularised. Further, frequency effects and the regularity-continuum effect that are observed in aphasic subjects can also be modelled. The model predicts that an aphasic profile with selectively impaired regular inflections would be evidence for a locally distinct processing of regular and irregular infections.
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Murtaza, Mariyam. "The role of Crumbs2 in neural development." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/2221/.
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The formation of a functionally integrated nervous system is dependent on a highly organized sequence of events that includes timely division and differentiation of progenitors. Three evolutionarily conserved polarity protein complexes are crucial for defining the apical and basolateral boundaries of cells. In my thesis, I demonstrate that one of the vertebrate homologs of Crumbs- Crumbs2 (Crb2) plays context dependent roles in the developing nervous system using two model systems: the chick embryonic hindbrain and the mouse embryonic telencephalon. In the developing telencephalon, conditional ablation of Crb2 leads to defects in recruitment of apical polarity proteins, cell junction proteins, positioning of mitotic cells and cortical neurogenesis. In the chick embryonic hindbrain, misexpression of Crb2 affects morphology of the neural tube and also affects the apical localization of cell polarity proteins, mitotic cell divisions and neural differentiation. In addition to this, I demonstrate that a novel secreted splice variant of Crb2 plays an important role in regulating neural crest cell migration. Taken together my analyses show that both loss and misexpression of Crb2 have similar effects on the apical domain and in confining mitotic cell divisions to the apical domain. This implies that the level of Crb2 is crucial for its various biological roles in the developing nervous system.
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Elms, Paul. "The role of the Zic genes in mouse neural crest development." Thesis, University of Oxford, 2004. http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff.
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Gacem, Nadjet. "Rôle d'ADAR1 dans le développement de la crête neurale." Thesis, Paris Est, 2019. http://www.theses.fr/2019PESC0016.
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Les cellules de le crête neurale sont une population de cellules précurseurs multipotentes qui émergent aux frontières du tube neural et de l’ectoderme non neural, migrent de manière extensive dans tout l'embryon et se différencient en une variété de types de cellules, notamment les cellules pigmentaires de la peau (mélanocytes), la glie du système nerveux périphérique (y compris les cellules de Schwann formant la myéline) et les neurones et les cellules gliales du système nerveux entérique. Chacune des étapes du développement de ces cellules est sous le contrôle de stimuli externes et de facteurs de transcription étroitement régulés formant un réseau complexe. Le rôle des modifications épigénétiques et post-transcriptionnelles a également été mis en évidence, mais leurs contributions aux troubles associés sont encore mal décrites. L'objectif de ma thèse était d'étudier le rôle de l'une des modifications post-transcriptionnelles les plus rependues : le RNA editing, dans le développement normal et pathologique de la crête neurale. Nous rapportons ici que ADAR1, enzyme responsable de la modification adénosine-inosine de l'ARN, est nécessaire au développement de trois dérivés de la crête neurale : les mélanocytes, les cellules de Schwann et le système nerveux entérique. L'invalidation conditionnelle spécifique d'Adar1 dans la crête neurale chez la souris provoque une dépigmentation généralisée et l'absence de myéline des nerfs périphériques résultant d'altérations affectant la survie des mélanocytes et de la différenciation des cellules de Schwann, respectivement. Des défauts de la glie entérique ont également été mis en évidence. Ces défauts sont tous trois précédés par l’activation d’une réponse immunitaire innée médiée par l’IFN. L’invalidation concomitante de MDA5, un senseur clé de détection d'ARNs non édités, corrige les défauts de myélinisation et de pigmentation observés chez les mutants adar1, suggérant qu'ADAR1, via son activité d’editing, protège ces dérivés de la crête neurale d'une production aberrante d’IFN délétère à leur survie ou différenciation. L’ensemble de ces résultats étendent le spectre d’action d’Adar1 au développement de la crête neurale normal et pathologiqueNeural crest cells are a population of multipotent precursor cells that emerge at the borders of the neural tube, migrate extensively throughout the embryo, and differentiate into a variety of cell types including the skin pigment cells (melanocytes), glia of the peripheral nervous system (including Schwann cells that form myelin) and the neurons and glia of the enteric nervous system. Each steps of the development of these cells is under the control of external stimuli and tightly regulated transcription factors that form a complex network. The role of epigenetic and post-transcriptional modifications was also highlighted, but their contributions to related disorders are still poorly described. The aim of my PhD project was to investigate the role of one of the most common post-transcriptional modification: the Adenosine to Inosine (A to I) RNA editing, in normal and pathologic NC development. Here, we report that adenosine deaminase acting on RNA (ADAR1), responsible for A to I editing of RNA, is required for regulating the development of three neural-crest derivatives: melanocytes, Schwann cells and enteric nervous system. Neural-crest specific conditional invalidation of Adar1 in mice led to global depigmentation and absence of myelin from peripheral nerves, resulting from alterations in melanocyte survival and late differentiation of Schwann cells respectively. Defects of enteric glia is also evidenced. These defects were preceded by upregulation of an innate immune inflammatory response. Simultaneous extinction of MDA5, a key sensor for the detection of unedited RNA, rescued the pigmentation and myelin defects of Adar1 mutants, suggesting that ADAR1 safeguards a subset of neural-crest derivatives from aberrant MDA5-mediated interferon production. We thus extend the landscape of ADAR1 function to the fields of neural-crest development and disease
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Moase, Connie E. (Connie Evelyn). "Cell interactions in abnormal neural tube and neural crest cell development of splotch mice." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70336.
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Early identification of mutant embryos prior to the manifestation of a defect facilitates the study of dysmorphogenesis. The In(l)lRk inversion was used as a cytogenetic marker to distinguish embryonic day 9 (D9) splotch (Sp) and splotch-delayed $(Sp sp{d})$ mouse mutants from heterozygous and wild-type littermates, and cellular aspects of abnormal neurulation and NCC migration were examined before inherent neural tube defects (NTDs) and deficiencies in neural crest cell (NCC) derivatives developed. In vitro analysis of NCC emigration from D9 neural tube explants revealed a delay in the release of NCCs from mutant neural tubes compared to controls, suggesting that the primary effect of the mutation was intrinsic to the neuroepithelium. Immunofluorescent localization of the neural cell adhesion molecule (N-CAM) antibody in situ demonstrated an increased intensity of antibody fluorescence in mutant tissue compared to controls, and further characterization by immunoblot analysis showed an altered embryonic N-CAM profile in both Sp and $Sp sp{d}$ mutants at D9 of gestation. The importance of N-CAMs in mediating cellular organization and communication has been well documented, supporting the idea that an alteration in this adhesion mechanism could result in the types of defects seen in splotch locus mouse mutants.
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Ringstedt, Thomas. "Neurotrophins during development : overexpression in neural stem cells /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980605ring.
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Agarwal, Pooja. "Transcriptional control of neural crest development by MEF2C." 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:3390029.
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Vais, Ricardo Silva dos Santos. "The Role of Microtubule nucleation during neural development." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668349.
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The γ-‐tubulin ring complex (γTuRC) is required to efficiently generate new microtubules (MT) in a process known as MT nucleation. In mitotic cells, MT nucleation by γTuRC occurs from the centrosome, in vicinity of the chromosomes and from the lattice of pre-‐ existing MTs in a process additionally involving the augmin complex. In neurons, the centrosome loses its MT nucleation capacity, while the γTuRC can still promote nucleation elsewhere. Still, it remains unclear how the γTuRC is regulated in these cells and whether other non-‐centrosomal sites function as microtubule-‐organizing centre in neurons.
The aim of this thesis is to understand how MT nucleation mediated by augmin and γTuRC contributes to brain development and how nucleation is regulated during this process.
In this thesis we show that the augmin complex is required for both axonal and dendritic development in vitro. In the axon, augmin guarantees that MTs are nucleated with the correct orientation, ensuring uniform axonal MT polarity. On the other hand, augmin depletion leads to an overall decrease in MT density in dendrites with no major effect on their polarity. Surprisingly, despite our findings, analysis of augmin function by other groups in vivo in flies and zebrafish has not revealed any dramatic defects.
Strikingly, we show that, in conditional KO mice with gene deletion in the augmin subunit Haus6 in neural progenitors, brain development is halted before embryonic day 13 and the animals die at birth. These major brain defects are caused by impaired mitosis and massive cell death in neuroprogenitors, indicating significant, species-‐specific differences in the requirement for augmin function.
In the last part of this thesis we identified KIF2A and CEP170 as γTuRC interactors in in vitro cultured mouse cortical neurons and we show that, in agreement with published data on KIF2A function, CEP170 seems to inhibit growth of axon collateral branches. We speculate that KIF2A and CEP170 may function as negative regulators of microtubules nucleation by γTuRC.
Together these results establish augmin-‐mediated nucleation as essential for mammalian brain development and provide first insight in the regulation of microtubule nucleation in neurons by γTuRC interactors.El complejo de anillo gamma-‐tubulina (γTuRC) es necesario para generar microtúbulos de manera eficiente en un proceso conocido como nucleación de microtúbulos. En células mitóticas, la nucleación a partir del γTuRC tiene lugar en el centrosoma, en regiones próximas a los cromosomas y en la superficie de microtúbulos previamente formados, en un proceso que requiere adicionalmente la presencia del complejo de augmina. A pesar de que en neuronas el centrosoma pierde su capacidad nucleadora de microtúbulos, el γTuRC aún puede inducir la nucleación en otros lugares. Sin embargo, aún se desconoce cómo se regula el γTuRC en estas células y si, aparte del centrosoma, existen otros lugares que puedan funcionar como centros organizadores de microtúbulos. El objetivo de esta tesis doctoral es entender cómo la nucleación de microtúbulos dependiente de augmina y del γTuRC contribuyen al desarrollo cerebral y cómo se regula la nucleación de microtúbulos durante este proceso. En esta tesis hemos demostrado que el complejo de augmina es necesario para el desarrollo de axones y dendritas in vitro. En el axón, augmina garantiza que los microtúbulos se nucleen en una orientación adecuada, asegurando una polaridad microtubular uniforme a lo largo del axón. Por otro lado, la ausencia de augmina causa una disminución general en la densidad de microtúbulos de las dendritas, sin afectar a su polaridad. Sorprendentemente, a pesar de nuestros descubrimientos, otros grupos han analizado la función de augmina in vivo (en moscas y pez cebra) sin encontrar ningún defecto significativo. Curiosamente, hemos observado que, en ratones knockout condicionales en los que la subunidad Haus6 de augmina ha sido delecionada de progenitores neuronales, el desarrollo cerebral se interrumpe antes del decimotercer día del desarrollo embrionario. Adicionalmente, esta condición resulta letal para los animales, que mueren durante el nacimiento. Se ha encontrado que las causas de estos dramáticos defectos cerebrales son problemas en mitosis y una muerte masiva de neuroprogenitores. Estos resultados indican que existen diferencias en el requerimiento de augmina entre diferentes especies. En la última parte de esta tesis identificamos KIF2A y CEP170 como interactores del γTuRC en neuronas corticales de ratones cultivadas in vitro. También demostramos que, en concordancia con datos publicados sobre KIF2A, CEP170 parece inhibir el crecimiento de ramificaciones laterales en axones. Nuestra hipótesis es que tanto KIF2A como CEP170 podrían actuar como reguladores negativos de la nucleación de microtúbulos dependiente de γTuRC. En conclusión, estos resultados demuestran que la nucleación dependiente de augmina es un proceso esencial en el desarrollo cerebral humano, y proporcionan una primera visión de cómo interactores del γTuRC pueden regular la nucleación de microtúbulos en neuronas.
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Coles, Brenda L. K. "Neural changes in forelimb cortex and behavioural development." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ38447.pdf.
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Garriock, Robert John. "Wnt11-Signaling Regulates Cardiac and Neural Crest Development." Diss., Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1655%5F1%5Fm.pdf&type=application/pdf.
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Coles, Brenda Louise Kay, and University of Lethbridge Faculty of Arts and Science. "Neural changes in forelimb cortex and behavioural development." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 1996, 1996. http://hdl.handle.net/10133/85.
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Neural changes in the forelimb cortex were studied at Postnatal (P) 10, 15, 20, 25, 30, and 100 days. Six biological markers of brain development, cortical thickness, Layer III pyramidal cell morphology, glial fibrillary acidic protein (GFAP), myelination, c-fos activity and Acetylcholinesterase (AChE) were correlated with the behavioural development of reaching, bimanual coordination, postural adjustment, and defensive feeding behaviours. The behaviours were filmed from P15 until P30 and then also in adulthood. For the behaviours there was a gradual development of the skilled patterns of paw and digit use seen in adults as well as in the patterns of movements in postural adjustment, carry behaviours and dodging and robbing type behaviours. The development of the adult patterns of movement were correlated to the morphological and biochemical changes in the cortex. The results suggest that the maturation of skilled movements depends upon anatomical and neurochemical maturation of the neocortex as well as upon learning.x, 132 leaves : ill. ; 28 cm.
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Sirois, Sylvain. "A neural network perspective on learning and development /." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36836.
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This manuscript-based thesis explores the relationship between learning and development. The first manuscript reviews the important empirical regularities identified in human discrimination shift learning, including a qualitative age-related change in performance observed in childhood. Leading theoretical accounts of the empirical data are discussed, suggesting that none provides a comprehensive interpretation. The manuscript presents the novel, spontaneous overtraining interpretation. It hypothesizes that age-related changes in human shift learning stem from differences in amount of processing. Successful neural network simulations of the reversal and nonreversal shift tasks and of the optional shift task are reported as tests of the hypothesis.The second manuscript reports simulations of additional discrimination shift tasks. These are the intradimensional and extradimensional shift tasks, in which novel stimuli are introduced in the relearning phase. Preschoolers and adults exhibit the same pattern of behavior in this variant of shift learning. Simulation results show that the spontaneous overtraining hypothesis captures this effect.
The third chapter reports an empirical validation of the shift learning model. If the shift learning performance of adults is a consequence of more extensive processing, it follows that adults in whom such processing is prevented should perform as preschoolers. Sixty adults took part in a shift learning experiment with a Brown-Peterson task as a cognitive load. Results mirror those observed with preschoolers. As a control, 40 adults performed the shift learning experiment without the cognitive load. These results replicate the typical adult performance. Overall, these experiments lend additional support to the model developed in Manuscript 1.
The final manuscript is a theoretical discussion of the relationship between learning and development. Two classes of neural networks are discussed, and their underlying assumptions about learning and development are highlighted. These are static architecture and generative architecture networks. It is argued that only generative algorithms, such as used in the shift learning simulations, qualify as developmental models. Both classes of networks are further contrasted with respect to innateness. The comparison suggests that only generative networks can acquire genuinely new representations. The manuscript proposes a novel formulation of Piaget's constructivism from the generative neural network perspective.
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Sales, Nicholas John. "Aspects of lexical development in artificial neural networks." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317984.
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England, S. J. "Morphogenetic analysis of neural development in the zebrafish." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598850.
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To understand vertebrate brain development we must determine how the cells of the simple, two-dimensional anterior neural plate are signalled to undergo complex reorganisation in to the elaborately structured, three-dimensional forebrain. To address this, I have collected time-lapse 3D movies of brain development in the optically transparent zebrafish embryo. I used these movies to accurately track the paths of many hundreds of cells representing the important cell territories of the brain, and so constructed dynamic, high-resolution fate maps of their transformations. My findings in wild-type embryos challenge the accepted model of forebrain folding. The resolution of bilateral eyes is not, as believed, achieved by the anterior-ward progression of the ventral diencephalon (hypothalamus) in the form of a neural keel, through the initially monocular eye field. The neural keel is actually formed by the hypothalamus moving deep than anterior-wards, subducting but not reshaping, more anterior progenitors of the dorsal forebrain (telencephalon) and medial eye field. In a novel observation, I can show that the separation of bilateral eyes occurs subsequent to this, coincident with the anterior-ward movement of dorsal diencephalic cells along the neural tube. I then used this new detailed model of normal development to address the causes of cyclopia – one consequence of the common human neural tube defect, holoprosencephaly (HPE). My analysis of time-lapse movies of animals with reduced Nodal or Wnt11 signalling – modelling HPE, identified two distinct morphogenetic events, whose failure can cause cyclopia. Under conditions of reduced Nodal signalling, cyclopia occurs because the cells moving deep to form the ventral midline are erroneously derived from eye territories anterior to the normal presumptive hypothalamus. In contrast, in mutant embryos with reduced Wnt11 signalling, cyclopia results from a reduced anterior-ward extension and movement of the future dorsal diencephalons, causing incomplete evagination of the optic lobes.
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Liu, Zhe. "The role of Robo in vertebrate neural development." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402169.
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Ward, Nicole J. "miRNAs and their role in neural crest development." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/65119/.
Full textAbstract:
The neural crest (NC) is a multipotent, migratory cell population that is unique to vertebrate embryos and gives rise to many derivatives, such as the craniofacial skeleton, sensory neurons and pigment cells. A complex gene regulatory network underlies the process of NC formation, which involves the early induction of the neural plate border (NPB), specification of the NC, migration of the NC away from the neural tube along distinct pathways and differentiation into diverse cell types. microRNAs (miRNAs) are a class of non-coding regulatory genes, which act posttranscriptionally to regulate gene expression. They are of widespread significance and have been implicated in many biological processes. Many miRNAs have now been identified, however, as of yet, they have not been shown to have any direct roles in early NC development. Using various molecular techniques this study has placed specific miRNAs within the complex NC gene network. These miRNAs are miR-196a and miR-219. SRNA sequencing of induced Xenopus NC tissue generated a miRNA expression profile which in combination with whole mount in situ hybridisation (WISH) revealed multiple candidate miRNAs expressed in NC. Using knockdown (KD) experiments, the depletion of miR-196a and miR-219 resulted in aberrant NC development including abnormal craniofacial cartilage development. Using luciferase assays, this study shows for the first time that miR-219 directly targets the transcription factor Eya1 in vitro. This gene lies directly upstream of the NPB marker Pax3. When miR-219 is knocked down, Pax3 expression is expanded across the surface ectoderm of the embryo suggesting the miR-219 serves to inhibit the Pax3 domain. To begin to understand the molecular mechanisms behind both this phenotype and why the NC is lost, RNA sequencing on dissected NC tissue was employed. Results from this sequencing data demonstrated that following miR-219 KD the NPB and the placodes form whilst the NC is lost. This indicates that miR-219 is playing a role in ensuring the correct specification of NC. In comparison, following miR-196a KD the NPB development is impaired and derivatives are lost (placode and NC). This implies miR-196a has an earlier role in ensuring the correct induction of the NPB possibly through fine-tuning early inducing signals such as BMP and Notch. Using the data presented in this study, the first models of how specific miRNAs could function in NC development have been formulated.
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Hatch, Victoria. "Transcriptional elongation is important for neural crest development." Thesis, University of East Anglia, 2013. https://ueaeprints.uea.ac.uk/48100/.
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Neural crest cells are a multipotent cell population, which migrate from the dorsal neural tube in early vertebrate development throughout the embryo to form a variety of cell types including pigment cells, craniofacial cartilage and sensory neurons [1, 2]. Here I show that the small molecule compound leflunomide is able to inhibit neural crest specification genes. Leflunomide exerts its actions by inhibiting pyrimidine synthesis and therefore RNA transcription [4]. Neural crest genes are thought to be actively transcribed and like many embryonic stem cell genes may undergo an increased level of transcriptional pausing and subsequent elongation rendering them more sensitive to the effect of leflunomide [3, 5]. I have gone on to show that components of the transcriptional elongation regulatory machinery, Cdk9 and CyclinT1 of the P-TEFb complex are also able to regulate neural crest specification. In particular the expression of the protooncogene c-Myc and c-Myc responsive genes are affected. c-Myc has been previously implicated in embryonic stem cell transcriptional elongation and also is well characterised to play a role in neural crest specification [6]. We postulate that regulation of c-Myc expression at the level of transcriptional elongation is important for the correct temporal and spatial development of the neural crest.
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Lin, Hsuan-Hwai. "Investigating the role of Neuronatin in neural development." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-role-of-neuronatin-in-neural-development(c7fad85a-bdaf-4d98-bc6b-8b465c8675bb).html.
Full textAbstract:
Neural induction is the process that occurs during embryogenesis whereby ectoderm is converted into neural tissue. However, the cellular and molecular mechanisms that govern this process are still not completely understood. For instance, in Xenopus, calcium signalling is known to play a pivotal role in neural induction but whether a similar mechanism occurs in mammals is unknown. As part of a wider study on genes regulating neural stem cell (NSC) development, we have discovered a novel role for Neuronatin (Nnaf), a regulator of intracellular Ca2+ concentration. In my thesis, I describe the use of a mouse embryonic stem cell (ESC)-derived neural differentiation model to dissect the function of Nnat in neural development. Using gain- and loss-of function experiments I show that ESCs in which Nnat expression had been knocked-down have a dramatically decreased ability to generate NSCs, and subsequently neurons, while ESCs that over-expressed Nnat generate an excess of NSCs and neurons. I reveal that Nnat interacts directly with the sarcoendoplasmic reticulum Ca2+-ATPase 2 (Apt2a2/SERCA2), and that Apt2a/SERCA inhibitors cause an increase in cytosolic calcium levels rescuing the ability of Nnat knockdown cells to generate neural cell-types. From these experiments I conclude that Apt2a/SERCA inhibition mimics the function of Nnat and, via the increase of cytosolic calcium, causes neural induction in Nnat knocked-down ESCs. I go on to show that this increase in cytosolic Ca2+, caused by inhibiting Apt2a/SERCA, activates Erk signalling and that inhibition of Erk signalling dramatically reduces the ability of ESCs to generate NSC. Together these results suggest that Nnat functions by increasing cytosolic Ca2+ levels, which in turn causes activation of Erk signalling leading to neural induction. In line with this, the expression of BMP4, which is an inhibitor of neural induction, was found to be up-regulated by Nnat knocked-down.
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Bydon, Mohamad. "Molecular genetic approaches to diseases of neural development." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-11212008-112418/.
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Eusebi, Silvia. "Creatine supplementation and neural plasticity in CNS development." Doctoral thesis, Urbino, 2018. http://hdl.handle.net/11576/2663607.
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Unal, Eroglu Arife. "REGULATION OF NEURAL CREST DEVELOPMENT REQUIRES FUNCTIONAL INTERACTIONS BETWEEN HDAC1, TFAP2A AND FOXD3." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1357141637.
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Osório, da Silva Liliana Alexandra. "Development of the caudal-most neural crest in the chick embryo." Paris 6, 2008. http://www.theses.fr/2008PA066208.
Full textAbstract:
La crête neurale (CN) issue de la région troncale du tube neural (TN) de l’embryon de poulet donne naissance aux neurones et cellules gliales du système nerveux périphérique et aux mélanocytes de la peau. Cependant, dans la région troncale la plus caudale (c) (niveaux somitiques 47 à 53), les cellules de CN (CCN) ne fournissent pas de neurones in vivo, ni en cultures in vitro (Catala et al. , 2000). Il en résulte l’absence de ganglions rachidiens alors que les motoneurones sont également absents dans cette région (Afonso & Catala, 2005). Afin d’élucider les causes de l’absence de dérivés neuraux de la CNc, nous avons entrepris d’analyser l’expression de plusieurs molécules impliquées dans les différentes étapes de la formation de cette structure. Nous avons trouvé que la plupart des acteurs moléculaires connus de la spécification de la CN sont présents dans la région dorsale du TNc dès que celui-ci est formé à E4, à l’exception de Msx1 qui n’est jamais exprimé à ce niveau. Néanmoins, seul un faible nombre de CCN migre dorsalement au TNc à E5. Ce défaut de migration semble être en rapport avec un défaut dans l’acquisition du phénotype mésenchymateux par les CCNc prospectives, qui pourrait être dû à une signalisation perturbée de BMP (maintien de Noggin) et de WNT (absence de Wnt1). Simultanément, une apoptose massive est détectée dans la moitié dorsale du TNc. La transplantation rostrale du TNc ou des somites montre que l’absence de dérivés neuraux est une propriété intrinsèque des CCNc et ne semble pas dépendre de l’influence des somites. L’expression ectopique de Noggin dans la région dorsale du TN troncal mime les caractéristiques des CCNc (faible nombre de cellules et absence des dérivés neuronaux). Enfin, nous avons évalué le rôle de Bmp4 et de ses cibles Msx1 et Wnt1 dans la spécification neuronale. L’ensemble de nos résultats montre que le TNc constitue un modèle précieux pour élucider les mécanismes moléculaires qui contrôlent l’émergence et différenciation des CCN.
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Зубенко, О. В., Л. М. Семенова, O. V. Zubenko, and L. M. Semenova. "Artificial Neural Networks and Their Current Level of Development." Thesis, Міжнародний гуманітарний університет; Південний регіональний центр Національної академії правових наук України, 2018. http://ir.lib.vntu.edu.ua//handle/123456789/24113.
Full textAbstract:
Neural networks, as one of the leading modern areas of information technology development, are reviewed in this work. The general concept of the neural network, the main types of them, as well their current level of development are presented.В роботі розглянуто нейронні мережі як один з провідних сучасних напрямків розвитку інформаційних технологій. Представлено загальну концепцію нейронної мережі, основні різновиди таких мереж та їх сучасний рівень розвитку.
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Enjin, Anders. "Neural Control of Movement : Motor Neuron Subtypes, Proprioception and Recurrent Inhibition." Doctoral thesis, Uppsala universitet, Genetisk utvecklingsbiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-147361.
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Movement is central for life, and all animals depend on accurate regulation of movement for purposeful behavior. There is great diversity of movements, ranging between simple and vital breathing movements to minute and subtle movements of the face used to communicate emotions. Consequently, motor neurons, which are the only route of central nervous system output, are essential for all motor behaviors. To control the many motor behaviors expressed by an animal, motor neurons are exposed to a large number and variety of modulating synaptic inputs and have evolved into subtypes with specific functions. In this thesis, motor neuron subtypes and the synaptic input to motor neurons from Renshaw cells and Ia afferents have been studied. Novel molecular markers that identify subtypes of motor neurons are described. Three markers, Chodl, Calca and ERRβ, have been used to study the degeneration of subtypes of motor neurons in a mouse model of the neurodegenerative disease amyotrophic lateral sclerosis (ALS). Another marker, 5-ht1d, has been used to record the electrophysiological character of gamma motor neurons. In mice that lack 5-ht1d, motor neurons develop with reduced proprioceptive input. Remarkably, these mice had fewer foot faults than control animals when challenged to cross a narrow beam suggesting that the amplitude of monosynaptic proprioceptive input to motor neurons is not essential for motor coordination. In a final set of experiments, genetic removal of vesicular transport of neurotransmitter from Renshaw cells suggest that Renshaw cells are not integral for motor circuit function or motor behaviors. However, they are involved in the development of motor circuits in the spinal cord. Together, this thesis provides novel molecular tools for studies of motor neuron subtypes and novel data regarding the development and function of spinal motor circuits.
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MacDonald, Jessica. "Methyl-CpG-Binding domain proteins and histone deacetylases in the stage-specific differentiation of olfactory receptor neurons." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/248.
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DNA methylation-dependent gene silencing, catalyzed by DNA methyltransferases (DNMTs) and mediated by methyl binding domain proteins (MBDs) and histone deacetylases (HDACs), is essential for mammalian development, with the nervous system demonstrating particular sensitivity to perturbations. Little is known, however, about the role of DNA methylation in the stage-specific differentiation of neurons. In the olfactory epithelium (OE), where neurogenesis is continuous and the cells demonstrate a laminar organization with a developmental hierarchy, we identified sequential, transitional stages of differentiation likely mediated by different DNMT, MBD and HDAC family members. Biochemically, HDAC1 and HDAC2 associate with repressor complexes recruited by both MBD2 and MeCP2. HDAC1 and HDAC2, however, are divergently expressed in the OE, a pattern that is recapitulated in the brain. Rather than simultaneous inclusion in a complex, therefore, the individual association of HDAC1 or HDAC2 may provide specificity to a repressor complex in different cell types. Furthermore, distinct transitional stages of differentiation are perturbed in the absence of MBD2 or MeCP2. MeCP2 is expressed in the most apical immature olfactory receptor neurons (ORNs), and is up-regulated with neuronal maturation. In the MeCP2 null OE there is a transient delay in ORN maturation and an increase in neurons of an intermediate developmental stage. Two protein variants of MBD2 are expressed in the OE, with MBD2b expressed in cycling progenitor cells and MBD2a in the maturing ORNs. MBD2 null ORNs undergo increased apoptotic cell death. There is also a significant increase in proliferating progenitors in the MBD2 null OE, likely due, at least in part, to feedback from the dying ORNs, acting to up-regulate neurogenesis. Increased cell cycling in the MBD2 null is also observed post-lesion, however, in the absence of feedback back from the ORNs, a phenotype that is recapitulated by an acute inhibition of HDACs with valproic acid. Therefore, disruptions at both transitional stages of ORN differentiation are likely in the MBD2 null mouse. Together, these results provide the first evidence for a sequential recruitment of different MBD proteins and repressor complexes at distinct transitional stages of neuronal differentiation.
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Haj, Fawaz Girgis. "CRYP#alpha# expression and ligand binding properties in the developing chick nervous system." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298627.
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Lee, Yuk Wa. "Characterization of Mab21l2 in neural development of vertebrate model /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20LEEY.
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Kadomatsu, Kenji. "The midkine family in cancer, inflammation and neural development." Nagoya University School of Medicine, 2005. http://hdl.handle.net/2237/5407.
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Ishikawa, Yuji, Takako Yasuda, Keiko Maeda, Atsuko Matsumoto, and Kouichi Maruyama. "Apoptosis in neural tube during normal development of medaka." Laboratory of Freshwater Fish Stocks Bioscience and Biotechnology Center Nagoya University, 2007. http://hdl.handle.net/2237/13834.
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Johansson, Amica. "Temporal regulation of neural stem cells during cortex development." Thesis, KTH, Skolan för bioteknologi (BIO), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215288.
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Milne, Charlotte Anne. "Analysis of neural development using ligand-trap transgenic lines." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444843/.
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Bone Morphogenetic Proteins (BMPs) are members of the Transforming Growth Factor-beta (TGF-beta) signalling protein superfamily. BMPs play important and diverse roles in cell-cell signalling, including establishing cell fate during the development of vertebrate embryos. Their activity is antagonised in vivo by a number of proteins such as noggin, which sequester BMP ligands, preventing them from binding to BMP receptors. This thesis describes studies to establish a binary genetic approach combined with a ligand trap system to manipulate BMP signalling in the frog embryo. This system has been used to investigate the roles of BMP signalling in dorso-ventral patterning of the forebrain Xenopus tropicalis. The binary system described utilises a variety of tissue- or region-specific gene promoters to drive expression of the GAL4 transcriptional activator. Such transgenic "driver" lines can be crossed with a "responder" line in which expression of a membrane-tethered fusion protein comprising human Noggin fused to GFP is regulated by a synthetic promoter responsive to GAL4 (UAS-flognog). Transient expression assays confirmed the effectiveness of the "responder" line, GAL4 transactivation of UAS-flognog resulted in the expression of Flognog and an expansion of neural progenitor tissue, indicated by the X-Sox3 marker. In a binary cross with the Otx2-gal4 driver line, targeted GAL4 transactivation lead to a decrease in phospho-Smad-1 staining in the anterior CNS and eye in a proportion of cross embryos. Such a cross resulted in embryos showing an open neural tube and alterations in both Pax6 (dorsal) and X-
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Hartley, K. "The role of BMPs in Xenopus anterior neural development." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603812.
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To determine the role of BMP signalling in neural development I chose to make use of the REMI transgenic technique. I cloned the Xenopus laevis Pax-6 promoter and used it as a tool to drive the expression of BMP4 and the ΔXBMPR (a dominant negative BMP receptor) in the anterior neural plate, from the end of gastrulation. The main conclusion I draw from the misexpression of BMP4 in transgenic Xenopus F0 embryos is that developing neural tissue is still competent to respond to BMP4 signalling at neural plate stages. Furthermore, BMP4 continues to function as an inhibitor of the majority of neural genes expressed into the neural plate stages of development, though not all neural genes are affected by the ectopic expression of BMP4 equally. In addition, I present evidence to suggest that the inhibition of BMP signalling by the misexpression of a truncated form of the BMP receptor in transgenic F0 embryos perturbs neural development. I also present evidence that BMP4 signalling is required for specifying the anterior border of the neural plate in Xenopus. I show that BMP4 and BMP7 are present in the prechordal mesoderm, a region underlying the midline of the anterior neural plate, which could receive the signalling molecules. In sum, I suggest that BMP signalling is involved in the fine-tuning of patterning and development of the neural plate. To further our understanding of the role BMPs play in neural development and to advance our technical abilities to misexpress factors, I have developed the Gal4-UAS system in Xenopus. I show that given factors can be transactivated in a precise manner, by the cross-fertilisation of transgenic founder lines. Additionally, I show that transactivation by Gal4 can result in a predicted phenotype for the effector gene in question.
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Wang, Qing. "Improving the cost model development process using neural networks." Thesis, De Montfort University, 2000. http://hdl.handle.net/2086/4196.
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In order to achieve success in export markets through provision of high levels of product choice, manufacturing industry will need to develop and economically use many new materials and manqfýcturing processes. To support this development, it is expected that the quantity, type, accuracy and complexity of cost models will need to be greatly increased. It is essential under these changing conditions that the process of developing cost models is able to remain responsive to user requirements and effective in terms of the resources required to generate models. This research investigates existing methods of establishing 'cost estimating relationships'and identifies their relative benefits and limitations in terms of their effects on the overall cost model development process. The basic tasks involved in the cost model development process and the basic characteristics of cost models have been identified and used to evaluate the use of Artificial Neural Networks (ANNs) as alternative methods of establishing cost models. The problem of identifying suitable ANN structures has been resolved by the use of the Taguchi Methodology. Experiments to identify the influence of varying the number of layers and number ofprocessing elements per layer within an ANN structure have shown that in general, increasing the number of processing elements per layer and decreasing the number of layers leads to increased estimating accuracy. Experiments to examine the effects of varying the amount of data used to develop the model and varying the number of variables within the model have indicated that substantial benefits, in terms of simplifying data identification and collection tasks can be realised when compared with regression analysis.
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Korsoni, Eleni. "The development and neural basis of visual re-entrance." Thesis, Birkbeck (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417061.
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Heath, Lindsay Anne. "Heterogeneity in neural crest development detected by monoclonal antibodies." Thesis, University of Southampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293618.
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Bernstein, Jacob (Jacob Gold). "Development of extracellular electrophysiology methods for scalable neural recording." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/107581.
Full textAbstract:
Thesis: Ph. D., Massachusetts Institute of Technology, School of Architecture and Planning, Program in Media Arts and Sciences, 2016.Cataloged from PDF version of thesis.
Includes bibliographical references.
In order to map the dynamics of neural circuits in mammalian brains, there is a need for tools that can record activity over large volumes of tissue and correctly attribute the recorded signals to the individual neurons that generated them. High-resolution neural activity maps will be critical for the discovery of new principles of neural coding and neural computation, and to test computational models of neural circuits. Extracellular electrophysiology is a neural recording method that has been developed to record from large populations of neurons, but well-known problems with signal attribution pose an existential threat to the viability of further system scaling, as analyses of network function become more sensitive to errors in attribution. A key insight is that blind-source separation algorithms such as Independent Component Analysis may ameliorate problems with signal attribution. These algorithms require recording signals at much finer spatial resolutions than existing probes have accomplished, which places demands on recording system bandwidth. We present several advances to technologies in neural recording systems, and a complete neural recording system designed to investigate the challenges of scaling electrophysiology to whole brain recording. We have developed close-packed microelectrode arrays with the highest density of recording sites yet achieved, for which we built our own data acquisition hardware, developed with a computational architecture specifically designed to scale to over several orders of magnitude. We also present results from validation experiments using colocalized patch clamp recording to obtain ground-truth activity data. This dataset provides immediate insight into the nature of electrophysiological signals and the interpretation of data collected from any electrophysiology recording system. This data is also essential in order to optimize probe development and data analysis algorithms which will one day enable whole-brain activity mapping.
by Jacob G. Bernstein.
Ph. D.
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Hemmati, Houman David Rothenberg Ellen V. "Neural stem and progenitor cells in cancer and development /." Diss., Pasadena, Calif. : Caltech, 2006. http://resolver.caltech.edu/CaltechETD:etd-05232006-140457.
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Gessaroli, Erica <1983>. "Development, degeneration and neural network of the bodily self." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6342/1/Gessaroli_Erica_tesi.pdf.
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The question addressed by this dissertation is how the human brain builds a coherent representation of the body, and how this representation is used to recognize its own body. Recent approaches by neuroimaging and TMS revealed hints for a distinct brain representation of human body, as compared with other stimulus categories. Neuropsychological studies demonstrated that body-parts and self body-parts recognition are separate processes sub-served by two different, even if possibly overlapping, networks within the brain.
Bodily self-recognition is one aspect of our ability to distinguish between self and others and the self/other distinction is a crucial aspect of social behaviour. This is the reason why I have conducted a series of experiment on subjects with everyday difficulties in social and emotional behaviour, such as patients with autism spectrum disorders (ASD) and patients with Parkinson’s disease (PD). More specifically, I studied the implicit self body/face recognition (Chapter 6) and the influence of emotional body postures on bodily self-processing in TD children as well as in ASD children (Chapter 7). I found that the bodily self-recognition is present in TD and in ASD children and that emotional body postures modulate self and others’ body processing.
Subsequently, I compared implicit and explicit bodily self-recognition in a neuro-degenerative pathology, such as in PD patients, and I found a selective deficit in implicit but not in explicit self-recognition (Chapter 8). This finding suggests that implicit and explicit bodily self-recognition are separate processes subtended by different mechanisms that can be selectively impaired.
If the bodily self is crucial for self/other distinction, the space around the body (personal space) represents the space of interaction and communication with others. When, I studied this space in autism, I found that personal space regulation is impaired in ASD children (Chapter 9).
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Gessaroli, Erica <1983>. "Development, degeneration and neural network of the bodily self." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6342/.
Full textAbstract:
The question addressed by this dissertation is how the human brain builds a coherent representation of the body, and how this representation is used to recognize its own body. Recent approaches by neuroimaging and TMS revealed hints for a distinct brain representation of human body, as compared with other stimulus categories. Neuropsychological studies demonstrated that body-parts and self body-parts recognition are separate processes sub-served by two different, even if possibly overlapping, networks within the brain.
Bodily self-recognition is one aspect of our ability to distinguish between self and others and the self/other distinction is a crucial aspect of social behaviour. This is the reason why I have conducted a series of experiment on subjects with everyday difficulties in social and emotional behaviour, such as patients with autism spectrum disorders (ASD) and patients with Parkinson’s disease (PD). More specifically, I studied the implicit self body/face recognition (Chapter 6) and the influence of emotional body postures on bodily self-processing in TD children as well as in ASD children (Chapter 7). I found that the bodily self-recognition is present in TD and in ASD children and that emotional body postures modulate self and others’ body processing.
Subsequently, I compared implicit and explicit bodily self-recognition in a neuro-degenerative pathology, such as in PD patients, and I found a selective deficit in implicit but not in explicit self-recognition (Chapter 8). This finding suggests that implicit and explicit bodily self-recognition are separate processes subtended by different mechanisms that can be selectively impaired.
If the bodily self is crucial for self/other distinction, the space around the body (personal space) represents the space of interaction and communication with others. When, I studied this space in autism, I found that personal space regulation is impaired in ASD children (Chapter 9).
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Mandal, Rakesh Kumar. "Development of Neural Network techniques to recognize handwritten characters." Thesis, University of North Bengal, 2015. http://ir.nbu.ac.in/handle/123456789/1790.
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