Thesis (Ph.D.)--University of Tennessee Health Science Center, 2006. / Title from title page screen (viewed on June 20, 2008 ). Research advisor: Seema Khurana, Ph.D. Document formatted into pages (xi, 154 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 127-139).

Commercial prosthetic feet weigh about 25% of their equivalent physiological counterparts. The human body has a tendency to overcome the walking asymmetry resulting from the mass imbalance by exerting more energy. A two link passive walking kinematic model, with realistic masses for prosthetic, physiological legs and upper body, has been proposed to study the gait pattern with unbalanced leg masses. The 'heel to toe' rolling contact has significant influence on the dynamics of biped models. This contact is modelled using the roll-over shape defined in the local co-ordinate system aligned with the stance leg. The effect of rollover shape curvature and arc length has been studied on various gait descriptors such as average velocity, step period, inter leg angle (and hence step length), mechanical energy. The bifurcation diagrams have been plotted for point feet and different gain values. The insight gained by studying the bifurcation diagrams for different gain and length values is not only useful in understanding the stability of the biped walking process but also in the design of prosthetic feet. It is proposed that the stiffness and energy release mechanisms of prosthetic feet be designed to satisfy amputee's natural gait characteristics that are defined by an effective roll-over shape and corresponding ground reaction force combinations. Each point on the roll-over shape is mapped with a ground reaction force corresponding to its time step. The resulting discrete set of ground reaction force components are applied to the prosthetic foot sole and its stiffness profile is optimised to produce a desired deflection as given by the corresponding point on the roll-over shape. It is shown that the proposed methodology is able to provide valuable insights in the guidelines for selection of materials for a multi-material prosthetic foot.

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Orientador: Gil Lucio Almeida / Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-05T08:56:07Z (GMT). No. of bitstreams: 1 Marconi_NadiaFernanda_D.pdf: 2668339 bytes, checksum: 84909294540d22968d0532a4f4fef14b (MD5) Previous issue date: 2005 / Resumo: Indivíduos portadores da Síndrome de Down melhoram o padrão muscular e cinemático de movimentos simples com o treinamento. Recentemente, demonstramos que indivíduos neurologicamente normais aumentam os impulsos do torque muscular do ombro e do torque de interação do cotovelo, com o treinamento de movimentos de reversão do braço. Neste estudo, verificamos se, com o treinamento, indivíduos portadores da Síndrome de Down usariam a mesma estratégia cinética para melhorar o desempenho de movimentos com reversão. Movimentos de reversão do braço realizados em três distâncias lineares diferentes foram reconstruídos utilizando um sistema óptico de análise de movimento. Os torques musculares e de interação foram calculados utilizando-se a dinâmica inversa. A atividade eletromiográfica dos principais músculos foi registrada. Ao contrário do esperado, indivíduos portadores da Síndrome de Down foram incapazes de aumentar a velocidade linear do dedo indicador, mesmo após 1.400 tentativas de prática. O mesmo ocorreu com os torques musculares e de interação das articulações ombro e cotovelo. No entanto, em oito sujeitos, um foi capaz de melhorar a velocidade dos movimentos de ida ao alvo e de volta à posição inicial. Esse sujeito foi capaz de aumentar o torque muscular do cotovelo e de interação do ombro com o treinamento. A melhora na velocidade dos movimentos desse sujeito não foi acompanhada de um aumento do erro. A incapacidade de indivíduos portadores da Síndrome de Down aumentarem as forças reativas (torque de interação do cotovelo) e musculares (torque muscular do ombro) com o treino, revela uma grande dificuldade desses sujeitos em tirar proveito de uma solução mecânica bastante eficiente. O fato de um único indivíduo ter apresentado uma melhora após usar uma estratégia ¿sub-ótima¿ do ponto de vista mecânico, demonstra que a Síndrome de Down pôde dificultar a elaboração de um modelo interno das forças que atuam na geração dos movimentos. Essa limitação talvez explique a dificuldade de esses indivíduos realizarem movimentos complexos e o aspecto desengonçado desses movimentos / Abstract: Individuals with Down syndrome improve the muscle activities and kinematics patterns of the single-joint movements with practice. Currently, we have showed that neurologically normal individuals increase the impulses of the shoulder muscle torque and elbow interaction torque with practice of the horizontal-planar arm movements with reversal. In this study, we verified if with practice, individuals with Down syndrome would be able to use the same kinetic strategy to improve the performance of the movements with reversal. Arm movements with reversal, performed on the three different target distances were reconstructed using a motion analysis system. The muscle and interaction torques were calculated using inverse dynamics. The EMG activities of the major muscles were collected. On the contrary that was expected, individuals with Down syndrome were not able to increase the linear speed of the fingertip after 1.400 trials of practice. The same was observed for the muscle and interaction torques for both shoulder and elbow joints. However, a one in eight subject was able to improve the velocity of both movements to and from the target. This subject also increased the impulses of the elbow muscle torque and shoulder interaction torque with practice. The improvement on the movement velocity was not accompanied the increase in the error ratio. The incapability of the individuals with Down syndrome to increase the reaction forces (interaction torque of the elbow) and muscle forces (muscle torque of the shoulder) with practice reveals a difficulty these subjects to get very efficient mechanical solution. The fact of the only one subject that showed improvement in velocity had used a sub-optimal strategy of the mechanical point of view, demonstrates that the Down syndrome can interfere on the elaboration of the internal model of forces that act on the movement generation. This limitation perhaps can explain the difficulty these individuals to perform complex movements and the clumsiness impression theses movements / Doutorado / Fisiologia / Doutor em Biologia Funcional e Molecular

The main focus of my PhD studies was aimed at understanding the general mechanism of nuclear translocation and isolating novel components of the nuclear translocation pathway in neurons. Using the Drosophila visual system as an in vivo model to study nuclear motility in developing photoreceptor cells (R-cells), I have identified a novel role for the Ser/Thr kinase Misshapen (Msn) and the endocytic trafficking pathway in regulating the nuclear translocation process. / The development of R-cells in the Drosophila eye disc is an excellent model system for the study of nuclear motility owing to its monolayer organization and the stereotypical translocation of its differentiating R-cell nuclei along the apical-basal plane. Prior to my thesis work, several laboratories had identified dynein and its associating proteins in R-cell nuclear translocation, however nothing was known about the signalling pathway that controlled their function in nuclear migration. Thus, one of my thesis goals was to elucidate the signalling mechanism controlling nuclear translocation in R-cells. / Using a combination of molecular and genetic approaches, I identified Msn as a key component of a novel signalling pathway regulating R-cell nuclear translocation. Loss of msn causes a failure of R-cell nuclei to migrate apically. Msn appears to control R-cell nuclear translocation by regulating the localization of dynein and Bicaudal-D (Bic-D). My results also show that Msn enhances Bic-D phosphorylation in cultured cells, suggesting that Msn regulates R-cell nuclear migration by modulating the phosphorylation state of Bic-D. Consistently, my results show that a Bic-D-phosphorylation-defective mutation disrupted the apical localization of both Bic-D and dynein. I propose a model in which Msn induces the phosphorylation of Bic-D, which in turn modulates the activity and/or subcellular localization of dynein leading to the apical migration of R-cell nuclei. / In addition to studying Msn, I have also searched for additional players in R-cell nuclear migration. From a gain-of-function approach, I found that the misexpression of the GTPase-activating-protein (GAP) RN-Tre caused a severe defect in R-cell nuclear migration. Since mammalian RN-Tre is involved in negatively regulating Rab protein activity, I speculated that the RN-Tre misexpression phenotype reflected a role for Rab-mediated vesicular transport in regulating R-cell nuclear migration. I systematically examined the potential role of Rab family proteins in R-cell nuclear migration and found that interfering with the function of Rab5, Rab11 or Shibire caused a similar nuclear migration phenotype. I propose that an endocytic pathway involving these GTPases is required for the targeting of determinants to specific subcellular locations, which in turn drive the apical migration of R-cell nuclei during development.

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