Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 130-169).

xiii, 104 p. : ill. (some col.) A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number. / Neurogenesis in Drosophila and mammals requires the precise integration of spatial and temporal cues. In Drosophila, embryonic neural progenitors, called neuroblasts, sequentially express the transcription factors Hunchback, Kruppel, Pdml/Pdm2 (Pdm) and Castor as they divide to generate a stereotyped sequence of neuronal and glial progeny. Hunchback is necessary and sufficient to specify the firstborn cell identity in many neuroblast lineages. Additionally, Hunchback is able to maintain an early-competence state in which early-born cells are generated. Furthermore, the Hunchback mammalian ortholog, Ikaros, possesses a similar ability to specify early- born cells in the vertebrate nervous system. However, the mechanisms underlying the function of Hunchback/Ikaros are unknown. Pdm and Castor are expressed later in many neuroblasts and can specify late-born neuronal cell identities in a model neuroblast lineage, NB7-1. Previous work studying their function in the NB7-1 lineage showed that Pdm and Castor act as repressors of Kruppel gene expression and inhibit the generation of the Kruppel-dependent cell identity. It is not known if the functions of Pdm and Castor are conserved across multiple neuroblast lineages during neurogenesis or whether these factors impart any restrictions on the ability of a factor like Hunchback to maintain early competence. To investigate the transcriptional mechanisms regulating early neuroblast competence in Drosophila, I have focused my dissertation research on two aims. The first is to examine the function of Pdm and Castor across multiple neuroblast lineages to characterize their potential roles as competence restricting factors; the second is to determine how Hunchback maintains early neuroblast competence and specifies early-born cell identities (e.g. as a transcriptional activator, repressor, or both). My work demonstrates that Pdm and Castor control the timing of Kruppel gene expression, and possibly the timing of other genes, in neuroblasts. Furthermore, I have shown that Hunchback acts as a transcriptional repressor of multiple target genes, including pdm and castor, to maintain early neuroblast competence. Because Hunchback must repress at least one additional unknown factor that can restrict neuroblast competence, I have piloted a screen to identify and characterize novel Hunchback target genes in the nervous system. This dissertation includes previously published and unpublished co-authored materials. / Committee in charge: Victoria Herman, Chairperson, Biology; Christopher Doe, Advisor, Biology; Judith Eisen, Advisor, Biology; Charles Kimmel, Member, Biology; Hui Zong, Member, Biology; Kenneth Prehoda, Outside Member, Chemistry

Orientador: Prof. Raphael Yokoingawa de Camargo / Dissertação (mestrado) - Universidade Federal do ABC, Programa de Pós-Graduação em Neurociência e Cognição, 2014. / Nowadays, utilizing co-processors, accelerators and specially GPGPU computation are widely accepted as a new paradigm of High Performance Computing (HPC). However, developing softwares that can utilize available resources still remains a challenging task. In other side, scientist have used legacy CPU-based simulators for decades and many of them are still the main tools in different fields of science. In fact, any activity that can combine the legacy simulators with powerful co-processors devices is in the main interest. In this project, we design and develop a simulation engine, Parallel Neural Network Simulator (PN2S), to communicate with MOOSE simulator (A well-known tools by Neuroscientists) and provide CUDA based execution for simulating realistic neural network models. The simulation engine maps the voltage distribution in neuron¿s body to sets of linear systems and solve them on GPU. To provide usable functionality, we also developed solver for active channels which support Hodgkin-Huxley model of ionic channels. We compared the engine with CPU version for both homogeneous simple models and randomly generated heterogeneous network. The evaluation focused on performance and also covered the accuracy of the simulation. The experimental results, showed that by facilitating PN2S engine, we can significantly increase the performance of a simulation engine, since its execution is quite transparent to the users and major parts of the host simulator.

Submitted by Luiz Augusto Rosa null (luiz.augusto.rosa@outlook.com) on 2018-03-19T12:34:56Z No. of bitstreams: 1 Dissertação - Luiz Augusto Rosa.pdf: 2095745 bytes, checksum: 4ecf357b59fc4edc60e2425328bf65b2 (MD5) / Rejected by Satie Tagara (satie@marilia.unesp.br), reason: Faltou a ficha catalográfica: anexar a ficha catalográfica na sequência da página de rosto (na versão impressa é no verso). on 2018-03-19T16:16:19Z (GMT) / Submitted by Luiz Augusto Rosa null (luiz.augusto.rosa@outlook.com) on 2018-03-19T18:55:21Z No. of bitstreams: 1 Dissertação Completa - Luiz Augusto Rosa.pdf: 2206500 bytes, checksum: 9e8f5f65501eb60ef2c7c0f6bb093043 (MD5) / Approved for entry into archive by Satie Tagara (satie@marilia.unesp.br) on 2018-03-19T19:35:12Z (GMT) No. of bitstreams: 1 rosa_la_me_mar.pdf: 2206500 bytes, checksum: 9e8f5f65501eb60ef2c7c0f6bb093043 (MD5) / Made available in DSpace on 2018-03-19T19:35:12Z (GMT). No. of bitstreams: 1 rosa_la_me_mar.pdf: 2206500 bytes, checksum: 9e8f5f65501eb60ef2c7c0f6bb093043 (MD5) Previous issue date: 2018-02-02 / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Nessa dissertação buscamos fazer uma análise filosófica das teorias sobre a emoção, sentimento, self e consciência de António Damásio frente ao contexto neurobiológico contemporâneo. No primeiro capítulo, nós fizemos uma revisão de literatura sobre os dois paradigmas da consciência vigentes na neurobiologia, no caso, o paradigma cognitivista, onde revisamos os trabalhos de Crick, Baars, Dehaene, Tononi, Koch e LeDoux, e o paradigma afetivista, onde revisamos as ideias centrais de Panksepp. No segundo capítulo, nós revisamos as ideias centrais de Damásio sobre emoção, sentimento, self e consciência, analisando tanto a atualização conceitual e neurobiológica no decorrer de suas obras principais quanto como cada teoria está embasada nas ideias de James sobre os processos emocionais e nos paradigmas discutidos no primeiro capítulo. No terceiro capítulo, nós revisamos as ideias centrais do modelo construtivista da emoção de Russell e Barrett, as posições de Damásio e outros autores sobre a problemática da possibilidade de consciência em animais não-humanos, avaliamos as teorias centrais de Damásio frente ao contexto neurobiológico atual, e analisamos tanto os problemas conceituais inerentes à teoria da consciência de Damásio quanto as posições de Damásio sobre o problema da causação mental e identidade mente-cérebro. Nós esperamos, com essa dissertação, ter contribuído, mesmo que modestamente, com um debate que vem ganhando grande impacto na literatura especializada, que vai muito além do aqui foi apresentado. / In this dissertation we sought to make a philosophical analysis of Antonio Damásio’s theories on emotion, feeling, self, and consciousness in the face of the contemporary neurobiological context. In the first chapter, we reviewed the literature on the two paradigms of consciousness in neurobiology, in this case, the cognitive paradigm, where we reviewed the works of Crick, Baars, Dehaene, Tononi, Koch and LeDoux, and the affectivist paradigm, where we reviewed Panksepp’s core ideas. In the second chapter we review Damasio’s central ideas on emotion, feeling, self, and consciousness, analyzing both the conceptual and neurobiological actualization in the course of his major works, and how each theory is based on James’ ideas on emotional processes and the paradigms discussed in the first chapter. In the third chapter, we reviewed the core ideas of Russell’s and Barrett’s constructivist model of emotions, the stance of Damasio and other authors on the problematic about the possibility of consciousness in nonhuman animals, we assessed Damasio’s central theories in the face of the current neurobiological context, and we analyzed both the conceptual problems inherent in Damasio’s theory of consciousness and Damasio’s stance on the problem of mental causation and mind-brain identity. We hope, with this dissertation, to have contributed, even modestly, to a debate that has been gaining great impact in the specialized literature, which goes far beyond what was presented here. / 2015/14849-3

Through an attractive hypothesis of work, we present the relaTionship between the frontal lobes and the neurobiological bases of Freud's psychoanalytic theory. We review and discuss the psycophysiological and clinical aproachs, in order to understand this relationship, arriving to the final examination of the organic and functional "disolutions" of the brain. We study and discuss the clinical progressive symptoms of the dementia and the differencial diagnosis of abnormal behavior, inrerpreted under the bases of Freud's theory. In this way it would be possible to arrive through some tempting interpretation of the psychopatic behavior, drug addiction and the last "syndrome of terrorism". / Se trata de establecer mediante una atractiva hipótesis de trabajo, las relaciones entre los lóbulo frontales y las bases neurobiológicas de la teoría freudiana del psicoanálisis. Se presenran y discuten las aproximaciones psicofisiológicas y clínicas, en la interpretación de estas relaciones, llegando al análisis final de las "disoluciones" orgánicas y funcionales del cerebro, pasando revista a los síntomas de la demencia y cuadros clínicos diferenciales, por los cuales se puede llegar a la interpretación freudiana de la psicopatía, la farmacodependencia y el síndrome del terrorismo.

Esta é uma investigação sobre a formação do arquiteto em sua dimensão sensível. A visão persistente de que ser artista é uma condição inata de alguns seres humanos tem gerado dificuldades na ação de criar, entre os aprendizes de arquitetura, à revelia das descobertas da Ciência sobre as capacidades cerebrais do ser humano, descobertas que interferem nas reflexões sobre como acontece o conhecimento. Ainda dificulta essa formação, um mundo atual consumista e negativamente pragmático que interfere na missão formadora da instituição escola de arquitetura, querendo forçá-la a ser mero curso profissionalizante. Esse panorama apresenta uma estrutura de formação sem a condição de poder alcançar a sensibilidade do aprendiz para fazê-lo perceber, intuir, criar espaços com sua dimensão que supera a função de abrigo das atividades humanas: sua condição de Arte. Este é o motivo desta Tese: propor uma modificação na fisionomia das estruturas vigentes de formação do arquiteto para que ela possa ser mais estimuladora da sensibilidade de seus aprendizes. / This is a research on architect formation in its dimension of Art. The predominant and persistent view that to be an artist is an innate condition of some human beings has been producing difficulties in the action of creation, among the apprentices of architecture, which ignore the science discoveries about the human beings brains. Another difficulty to this formation is the present consumer and pragmatic world which interferes on the formative mission of the school of architecture institution, pretending enforced it to be a mere professional course. This scene presents a formation structure without a condition that could allow to reach the sensibility of the apprentice in order to make him perceive, feel, create spaces with his own dimensions which overcome the function of sheltering human activities: its Art dimension. This is the leitmotiv of this thesis: to propose another physiognomy to the present structure for the architect formation as a way to make it more stimulating to the sensibility of its apprentices.

Orientador: Claudio Antonio Barbosa de Toledo / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-09T19:38:46Z (GMT). No. of bitstreams: 1 Santana_RenatoFigueiredode_M.pdf: 3137636 bytes, checksum: bfb0cb5b3693de7bf1e46cd7ce5de3db (MD5) Previous issue date: 2007 / Resumo: Glutamato, um dos principais neurotransmissores excitatórios do sistema nervoso central participa do tráfego de informação neural nos núcleos de base de aves e mamíferos através de receptores ionotrópicos do tipo AMPA. Investigamos a variação da expressão das subunidades que compõem esse receptor em áreas motoras telencefálicas do encéfalo de pombos (C. lívia) em diferentes idades: do nascimento até 10 dias de vida e na idade adulta. As aves foram perfundidas e seus cérebros foram processados por imunohistoquímica usando anticorpos contras as subunidades GluR1 e GluR4 e contra um epítopo comum às subunidades GluR2 e GluR3 (GluR2/3); além disso, anticorpos contra proteínas ligantes de cálcio foram utilizados como marcadores. O globo pálido (GP) apresentou marcação crescente de neurônios GluR1+ durante os primeiros dias de vida, atingindo pico em P3, decaindo em seguida e sendo novamente expresso na fase adulta. A expressão de GluR2/3 mostrou-se relativamente estável no GP durante os primeiros dias de vida, mas decaiu após P3. Células expressando GluR4 foram principalmente evidentes entre P3 e P7 no GP. Com relação ao corpo estriado, a neurópila estriatal foi intensamente marcada para GluR1 e GluR2/3, contrastando com a pobre marcação de neurópila apresentada pelo globo pálido. Nos diferentes estágios de desenvolvimento a neurópila estriatal foi pobre em GluR4. O número de células GluR1+ no corpo estriado mostrou pico máximo em P5 e o de GluR2/3+ foi crescente ao longo das idades. A região lateral do estriado lateral indicou marcação semelhante à região central em todas as idades, com padrão estável de crescimento para GluR2/3, um pico em P5 para GluR1 e escassa presença de marcação GluR4+ em todas as idades. O número de células PV+ decai durante o desenvolvimento e CB foi expressa nos gânglios da base somente na fase adulta. Nossos resultados indicam que subunidades do receptor de glutamato do tipo AMPA são diferencialmente expressas durante o crescimento pós-natal. Estas alterações podem estar relacionadas com mudanças funcionais que conduzem à estruturação final da circuitaria sináptica envolvida nas respostas motoras desta espécie, cujo desenvolvimento até o estágio de auto-suficiência depende dessa habilidade / Abstract: AMPA-type glutamate receptors mediate the responses of neurons of the striatal part of the basal ganglia to excitatory cortical input in both birds and mammals. We have investigated the maturation of the expression of the four AMPA receptor subunits in 42 pigeons (C. livia) at different stages, from hatching (P0) to 1, 3, 5, 7, or 10 days posthatch (P1-10), to adulthood. Pigeons are altricial, become relatively mobile by 12 days, and independent by one month. The birds were perfused and their brains processed by standard immunolabeling using antibodies against the GluR1 or GluR4 subunits, or against an epitope common to both GluR2 and GluR3 (GluR2/3) subunits. Antibodies against calcium binding proteins parvalbumin (PV) and calbindin (CB) were used as neuronal marker. Globus pallidus at P0 showed labeling in neurons for GluR1 and GluR2/3, which reached its peak at P3. The GluR1 perikaryal labeling in globus pallidus decreased after P5, but was labeling another time at adulthood. GluR2/3 remained stable into early age, but decrease after P3. The perikarya of globus pallidus and their processes were also labeled for GluR4 at P0, and GluR4 cells GluR4+ was peak between P3 and P7. PV was decrease during the development. CB was expressed in basal ganglia only at adulthood. At P0, the striatal neuropil was intensely (though diffusely) labeled for GluR1 and GluR2/3, which contrasted distinctly with the poor neuropil labeling for both in globus pallidus. GluR1+ was peak at P5 and GluR2/3 increase during the time. At all stages, the striatal neuropil immunolabeling was poor for GluR4, although neurons were labeled for GluR4. GluR4 was peak at P7. PV was peak at adult age. The labeling of GluR2/3 in lateral region of lateral striatun was similar to central region, but GluR1+ was increase by ages. Our results indicate that AMPA receptor subunits was expressed differentially at the development post-hatching. This may support maturational changes that facilitate the motor development of this altricial species / Mestrado / Fisiologia / Mestre em Biologia Funcional e Molecular

A conversão da proteína príon celular (PrPc) em sua isoforma anormal PrPsc está associada a uma série de doenças neurodegenerativas, genericamente designadas por doenças priônicas. Embora a literatura tenha enfatizado o estudo do PrPsc e o mecanismo de propagação das doenças de príon, pouco tem sido feito para o entendimento do papel fisiológico do PrPc. Em 1997 nosso grupo descreveu um receptor/ligante para o PrPc utilizando o princípio da hidropaticidade complementar. Neste trabalho isolamos e identificamos este ligante de PrPc como sendo a STI-1 (Stress Inducible Protein-1). In vitro, a STI-1interage com o PrPc de maneira específica, saturável e com alta afinidade (Kd=8x10-8M). Paralelamente, mostramos que o PrPc se liga ao domínio RNIAEIIKDI da laminina (Ln) (Kd=2x10-8M). O bloqueio de PrPc na superfície de neurônios hipocampais de embriões de ratos e camundongos, reduziu a neuritogênese induzida por Ln. Além disso, neurônios provenientes de animais PrP -/- são incapazes de estender neuritos sobre o peptídeo RNIAEIIKDI, sugerindo que o PrPc é o único receptor celular para este domínio da Ln. Estes dados indicam que a interação PrPc-Ln seja relevante nos fenômenos de adesão e diferenciação neuronais. A caracterização das interações PrPc-Ln e PrPc-STI-1 representa contribuições importantes para a elucidação do papel biológico do PrPc. / Conversion of the cellular prion protein (PrPc) to its abnormal isoform PrPsc is associated with some neurodegenerative and fatal diseases called prion diseases. Although the literature has been emphasizing the mechanism of PrPsc conversion and illness propagation, little attention has been given to the PrPc physiological role. In 1997, our group described a PrPc receptor/ligand based on the complementary hydropathy theory. Herein, we identify the PrPc receptor/ligand as STI-1, the Stress Inducible Protein-1. In vitro studies showed that STI-1 is a specific, saturable and high affinity ligand for PrPc (Kd=8x10-8M). In parallel, we demonstrated that PrPc interacts with RNIAEIIKDI domain of laminin (Ln) (Kd=2x10-8M). The blockage of PrPc, both from embryonic rats and mice hippocampal neuros, inhibited Ln-induced neurite outgrowth. In addition, neurons from PrPc null mice are unable to extend neurites on RNIAEIIKDI, suggesting that PrPc is the unique cellular receptor for this Ln domain. These data indicate that PrPc-Ln interaction is relevant for neuronal adhesion and differentiation. The characterization of PrPc-Ln and PrPc-STl-1 interactions represents important contributions for the elucidation of the PrPc physiological role.

O mundo ainda está enfrentando uma crise financeira, que começou em meados de 2007 e até o momento está longe de ser resolvida. Os mercados de ações ao redor do mundo reagiram mal e as notícias em tempo real nunca desempenharam um papel tão importante para os investidores, como visto nesta crise. Em outras palavras, o impacto dos meios de comunicação aprofundou a dinâmica de baixa dos mercados financeiros, o que é amplificada pela volatilidade intrínseca do mesmo. Assim, a Neuroeconomia veio como um novo campo de questionamentos, o qual tem a finalidade de estudar a tomada de decisão, tendo em conta o papel desempenhado pela emoção e seus aspectos fisio-patológicos. Se utiliza neste estudo uma amostra de oitenta (80) pessoas, classificados em quarenta alunos de graduação e quarenta (40) trabalhadores experientes do mercado financeiro (traders), ambos igualmente divididos em 50% do sexo masculino e 50% do sexo feminino. O escopo é de avaliar o envolvimento de uma ampla rede de circuitos neurais envolvidos na avaliação de riscos, benefícios e conflitos (esta ponderação está intimamente relacionada à serotonina em caso de riscos e benefícios no caso de dopamina) para cada grupo a fim de verificar como reagem neste ambiente. Compreender a funcionalidade de tais sistemas é de fundamental importância para a compreensão da dinâmica do mercado financeiro e de suas anomalias, ou seja, para registrar a percepção de cada indivíduo em relação ao sentimento geral do mercado, seja ele a favor ou adverso. Portanto, o principal objetivo desta tese é mapear a atividade cerebral usando uma técnica desenvolvida por Rocha (2001, 2004 e 2010), operando uma simulação de negociação da Bolsa de Valores BMF&Bovespa, a fim de compreender melhor a neurodinâmica do processo de decisão no mercado de capitais / The world is still facing a financial crisis, which started in mid 2007 and up to now is far from being solved. Stock markets around the world reacted badly and the real time news has never played such an important role to investors as seen in previous crisis. In other words, the impact of the media deepened the bear dynamics of the markets, that is, it amplified the volatility of it. Thus, Neuroeconomics comes as a new field of inquiring that has the purpose of studying decision making taking into consideration the role played by emotion and its physio-pathological aspects. Here, it is used a sample of eighty (80) volunteers, sorted out into forty undergraduate students and forty (40) experienced financial market practioneers (namely traders), both equally divided into 50% male and 50% female. The scope is to evaluate the involvement of a wide network of neural circuits involved in risk assessments, benefits and conflicts (this weighting is closely related to the serotonin neural circuits in the event of risks and benefits in the case of dopamine) so as to verify how both groups react to this environment. Understanding the functionality of such systems is of fundamental importance for understanding the dynamics of the financial market and its anomalies, ie to record the perception of each individual in relation to the general market sentiment, being it in favour or on the contrary, adverse. Therefore, the main objective of this thesis is then to map brain activity using a technique developed by Rocha et al (2001, 2004 and 2010), operating a simulation of trading within the BMF&Bovespa, in order to better understand the process of neurodynamics decision making in the capital market

M.A. (Psychology) / Sudden Infant Death Syndrome is the most prevalent cause of death in infants between one and twelve months of age. Most deaths attributed to Sudden Infant Death Syndrome occur between 1 and 4 months of age. There is a marked decrease after this age in the number of deaths classified as Sudden Infant Death Syndrome. It is usually defined as the sudden death of any infant usually during sleep which is unexpected by history and in which a thorough postmortem examination tails to demonstrate an adequate cause tor death (Foundation for the Study of Infant Deaths, 1989) • Epidemiologic, pathologic and physiologic data suggest the mechanism ot Sudden Infant Death Syndrome is complex, characterized by interaction at many levels ot the neural axis, between the organism and the environment and spanning both pre- and post-natal lite. Observations suggest that the Sudden Infant Death Syndrome infant has experienced adverse influences prenatally Which may make him peculiarly vulnerable to postnatal environmental stress (Valdes Dapena, 1988). However, the specific nature and cause of this condition continues to elude both scientists and practitioners. In the last few years research has shed some light on various epidemiologic aspects of the problem, on pathologic anatomy and on clinical issues such as the relative importance of spontaneous, prolonged, idiopathic apnea. Some Sudden Infant Death Syndrome victims showed evidence of neonatal brain dysfunction, including abnormalities in respiration, feeding and temperature regulation and have been shown to have pathologic abnormalities consistent with chronic hypoxia (Kelly' Shannon, 1982). Once again, however, the research appears not to be conclusive, leaving many unanswered questions...