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1

Griveau, Amélie. "Characterization and function of Dbx1-derived Cajal-Retzius cells during cerebral cortex development." Paris 6, 2009. http://www.theses.fr/2009PA066265.

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Notre premier travail porte sur la théorie des classes de Chern pour les faisceaux cohérents. Sur les variétés projectives, elle est complètement achevée dans les anneaux de Chow grâce à l'existence de résolutions globales localement libres et se ramène formellement à la théorie pour les fibrés. Un résultat de Voisin montre que ce résolutions n'existent pas toujours sur des variétés complexes compactes générales. Nous construisons ici par récurrence sur la dimension de la variété de base des classes de Chern en cohomologie de Deligne rationnelle pour les faisceaux cohérents en imposant la formule de Grothendieck-Riemann-Roch pour les immersions et en utilisant des méthodes de dévissage. Ces classes sont les seules à vérifier la formule de fonctorialité par pull-back, la formule de Whitney et GRR pour les immersions; elles coïncident donc avec les classes topologiques et les classes d'Atiyah. Elles vérifient aussi GRR pour les morphismes projectifs. Notre second travail est l'étude des schémas de Hilbert ponctuels d'une variété symplectique ou presque-complexe de dimension 4. Ils ont été construits par Voisin et généralisent les schémas de Hilbert connus pour les surfaces projectives. En utilisant les structures complexes relatives intégrables introduites dans la construction de Voisin, nous pouvons étendre au cas presque-complexe ou symplectique la théorie classique. Nous calculons les nombres de Betti, nous construisons les opérateurs de Nakajima, nous étudions l'anneau de cohomologie de ces schémas de Hilbert et nous prouvons dans ce contexte un cas particulier de la conjecture de la résolution crêpante de Ruan.
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2

Weragalaarachchi, Krishanthi Tharanga Harshani. "Morphological Study of Dbx1+ Respiratory Rhythm-Generating Neurons in PreBoetzinger Complex in Neonatal Mice." W&M ScholarWorks, 2012. https://scholarworks.wm.edu/etd/1539626922.

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3

Vann, Nikolas C. "Role of Dbx1-Derived Pre-Bötzinger Complex Interneurons in Breathing Behaviors of Adult Mice." W&M ScholarWorks, 2017. https://scholarworks.wm.edu/etd/1530192336.

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Breathing is a rhythmic motor behavior essential to sustain homeostasis and life itself in humans and all terrestrial mammals. A specialized neuronal network is responsible for generating and controlling the rhythm and pattern for breathing. The core rhythm-generating microcircuit in particular is located within a site dubbed the preBötzinger complex (preBötC). The preBötC is a heterogeneous region containing neurons with both respiratory and non-respiratory activity that express excitatory and inhibitory transmitters, peptide transmitters and peptide receptors. More recently, preBötC neurons have been characterized by molecular genetics. The markers historically used to define the respiratory CPG within the preBötC intersect with an embryonic transcription factor, developing brain homeobox 1 (Dbx1). Our lab, and our French colleagues, hypothesized that neurons derived from the Dbx1-expressing precursor cells (hereafter referred to as Dbx1 neurons) form the core microcircuit for inspiration breathing rhythm, that is, the Dbx1 core hypothesis. Evidence from many labs supports the role of the Dbx1 core hypothesis at embryonic and neonatal stages of development. However, the role of Dbx1 neurons in adult animals remains incompletely understood. Furthermore, contemporary data suggests the portfolio of functions for brain stem Dbx1 neurons includes premotor and arousal-related functions, which casts doubt on the veracity of the Dbx1 core hypothesis. Here I investigate the role of Dbx1 neurons in adult animals with intact sensorimotor integration systems using intersectional mouse genetics to express light-responsive membrane proteins to excite or depress Dbx1 neurons while simultaneous measuring breathing. Using these light-sensitive proteins to manipulate Dbx1 neuron function, I offer evidence that affirms the Dbx1 core hypothesis by depressing or stopping breathing, enhancing breathing, and altering breathing timing. I conclude that .... Knowing the cellular point of origin for breathing behavior gives us a target to study the cellular and synaptic mechanisms this key physiological behavior and provides general insight into rhythmic networks and physiological brain function.
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4

Teissier, Anne. "L'évolution du néocortex des Mammifères : gène Dbx1 et les cellules transitoires de la plaque corticale." Paris 6, 2010. http://www.theses.fr/2010PA066336.

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L’évolution du cerveau chez les mammifères à permis l’augmentation du nombre de neurones et la formation d’un néocortex en six couches. Au cours du développement du télencéphale de la souris, le facteur de transcription Dbx1 est exprimé aux stades précoces de la neurogénèse par des progéniteurs palliaux présents à la frontière entre le pallium et le sous-pallium (PSB). Nous avons caractérisé par traçage génétique une nouvelle population de cellules glutamatergiques dérivant des progéniteurs exprimant Dbx1 à la PSB et migrant tangentiellement dès E11. 5 pour peupler l’ensemble du pallium à E14. 5. Cette population se distribue de façon homogène dans la plaque corticale (PC) de l’ensemble du neocortex à la naissance avant de mourir massivement par apoptose durant la première semaine postnatale. L’ablation génétique de ces cellules induit la différenciation précoce des progéniteurs corticaux conduisant à une diminution du nombre total de neurones générés. La cinétique de ces défauts nous permet de suggérer que ces cellules transitoires envoient des signaux pendant leur migration pour maintenir les progéniteurs dans un état de prolifération. L’expression du gène Dbx1 à la PSB étant spécifique des mammifères, l’acquisition de cette nouvelle population pourrait donc être à l’origine de l’augmentation du nombre de neurones dans le cortex cérébral
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5

Song, Hanbing. "Rhythmogenic and Premotor Functions of Dbx1 Interneurons in the Pre-Bötzinger Complex and Reticular Formation: Modeling and Simulation Studies." W&M ScholarWorks, 2016. https://scholarworks.wm.edu/etd/1499449835.

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Breathing in mammals depends on rhythms that originate from the preBötzinger complex (preBötC) of the ventral medulla and a network of brainstem and spinal premotor neurons. The rhythm-generating core of the preBötC, as well as some premotor circuits, consists of interneurons derived from Dbx1-expressing precursors but the structure and function of these networks remain incompletely understood. We previously developed a cell-specific detection and laser ablation system to interrogate respiratory network structure and function in a slice model of breathing that retains the preBötC, premotor circuits, and the respiratory related hypoglossal (XII) motor nucleus such that in spontaneously rhythmic slices, cumulative ablation of Dbx1 preBötC neurons decreased XII motor output by half after only a few cell deletions, and then decelerated and terminated rhythmic function altogether as the tally increased. In contrast, cumulatively deleting Dbx1 premotor neurons decreased XII motor output monotonically, but did not affect frequency nor stop functionality regardless of the ablation tally. This dissertation presents several network modeling and cellular modeling studies that would further our understanding of how respiratory rhythm is generated and transmitted to the XII motor nucleus. First, we propose that cumulative deletions of Dbx1 preBötC neurons preclude rhythm by diminishing the amount of excitatory inward current or disturbing the process of recurrent excitation rather than structurally breaking down the topological network. Second, we establish a feasible configuration for neural circuits including an Erdős-Rényi preBötC network and a small-world reticular premotor network with interconnections following an anti-preferential attachment rule, which is the only configuration that produces consistent outcomes with previous experimental benchmarks. Furthermore, since the performance of neuronal network simulations is, to some extent, affected by the nature of the cellular model, we aim to develop a more realistic cellular model based on the one we adopted in previous network studies, which would account for some recent experimental findings on rhythmogenic preBötC neurons.
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6

BURGMAN, BRANDON MICHAEL. "DISCOVERING GENETIC INTERACTIONS OF THE DEAD-BOX PROTEIN, DBP1." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/618701.

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Medulloblastoma is the single most common form of malignant brain cancer in children. A molecular understanding of the cellular processes that leads to its formation is imperative in order to design treatments or a cure to this deadly cancer. A recent genomic screening of medulloblastoma patients showed high mutation rates of the gene DDX3X indicating a possible connection to the cancer. Thus, we investigated a yeast ortholog of DDX3X, Dbp1, to gain some insight of the function of the protein within the cell and its role in medulloblastoma formation. In order to gain deeper understanding of this mostly uncharacterized DEADbox RNA helicase, previous lab members perfor med a synthetic lethal screen in Saccharomyces cerevisiae with dbp1null cells. We found that a wild type copy of SHM2, was found to rescue sectoring in one of these synthetic let hal yeast strains. However, it has been documented that shm2 mutations show synthetic lethal interactions with ade3 mutations, so we are unable to conclude that SHM2 has genetic interaction with DBP1. However, this finding can be used to rule out SHM2 as the cause of loss of sectoring phenotype in other dbp1 synthetic lethal mutant strains.
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7

Hett, Anne. "Studies on the metabolism of retained and excised introns in human cells." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/10515.

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In eukaryotes the coding regions of most genes are interrupted by introns that must be removed by splicing to form a coding mRNA. However, while the splicing mechanism has received a lot of attention, much less is known about the metabolism of introns. This is partly due to the difficulties in studying introns as both aberrantly spliced transcripts and spliced introns are rapidly degraded. In this study, I have analysed intron metabolism in two respects: first I have investigated how introns are degraded following the completion of splicing. Second, I investigate the fate of transcripts, in which introns are retained due to splicing failure. In order to study the degradation of introns following splicing, I performed siRNA mediated knock down of the debrancing enzyme (Dbr1). Following splicing, introns are present in a circular lariat structure and Dbr1 is the enzyme thought to be responsible for opening this. Indeed, I found that knockdown of Dbr1 increased the amount of stabilised introns. Interestingly, introns were found to be stabilised in the cytoplasm and not in the nucleus as expected, even though immunofluoresence showed that Dbr1 is clearly nuclear. However, western blot analysis localised Dbr1 in the cytoplasm. Further investigation showed widely used methods to separate nuclear and cytoplasmic fractions are prone to generating artefacts which result in nucleoplasmic proteins delocalised to the cytoplasm. This finding may prevent future misinterpretation of data obtained by these methods. To investigate splicing failure, it was necessary to generated a sufficiently large pool of unspliced transcripts. To do this I used antisense morpholinos (AMOs) that bind to specific snRNAs (small nuclear RNAs). They are designed to block interaction surfaces that are important for splicing. Using this approach, I investigated the localisation of RNA transcripts and selected RNA processing and degradation factors in normal conditions and where splicing was inhibited. When splicing is inhibited I found splicing factors and unspliced, polyadenylated RNA localising to nuclear, splicing speckle marker SC35 positive speckles. I further discovered that for RNA to localise to nuclear speckles, polyadenylation and RNA cleavage are essential, indicating that SC-35 speckles might sequester unspliced transcripts preventing translation of potentially harmful transcripts. These transcripts remain functional however, and can be spliced where functional spliceosomes can be assembled.
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Cairns, Mari. "Identity and its relationship with borderline symptoms : the development of an identity questionnaire." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:b9a4f78e-dbf1-4586-af90-4a5e57d82e55.

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Clinical and theoretical literature suggests that some people who present with psychological problems have a poorly developed sense of their own identity. It has also been suggested that cognitive theory and therapy does not always adequately identify, conceptualise, and address these identity problems. The current study aims to develop a self-report questionnaire measure to assess these identity problems. It also tests some specific hypotheses about the relationship between identity problems and other psychological constructs, including borderline personality disorder symptomatology. anxiety and depression.
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Kent, Louisa. "The molecular pathogenesis of FUS mutations in amyotrophic lateral sclerosis using in vivo and in vitro models." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:f0968f9d-db01-4ace-bbd7-fc43319e19ea.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterised by degeneration of both upper and lower motor neurons. Most ALS occurs in a sporadic manner, though 5-10% is familial. Fused in sarcoma (FUS) is an RNA binding protein, and mutations in the FUS gene are responsible for approximately 4% of familial and < 1% of sporadic ALS cases. This work uses in vitro and in vivo models to examine the cellular effects of FUS mutations and the potential mechanisms of motor neuron toxicity. The first section describes a family with a severe clinical form of ALS due to a FUS truncation mutation p.G504Wfs*12. This mutation demonstrates a severe phenotype in vitro, with mislocalisation of mutant FUS from the nucleus to the cytoplasm, and co-localisation with stress granules. Comparing these results with other mutations highlights the correlation between FUS mislocalisation and clinical phenotype, suggesting that the distribution of FUS plays a role in the pathogenesis of ALS. The next section explores the phenotype of primary motor neurons from a FUS BAC transgenic mouse model expressing low levels of wild-type or P525L human FUS. P525L-FUS shows marked mislocalisation to the cytoplasm and co-localisation with stress granules, with evidence of reduced survival and alterations in stress granule dynamics. This suggests that motor neurons expressing mutant FUS show inherent vulnerability. The final section explores transcript levels and alternative splicing in both FUS and TDP-43 BAC transgenic mouse models. Key proteins such as TDP-43, FUS and SMN show alterations in mRNA levels in CNS tissue, and some subtle splicing alterations are described. This work suggests that mutations in FUS are likely to affect motor neurons even when expressed at very low levels. Alterations in FUS distribution, stress granule dynamics, and regulation of transcription may all play a part in conferring a susceptibility to developing ALS.
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10

Magni, Martina. "Functional characterization of the human protein deleted in breast cancer 1 (DBC1) involvement in the DNA damage response." Thesis, Open University, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701431.

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The DNA damage response (DDR) is an intricate signalling network established by eukaryotic cells in order to manage the insults to their DNA, arising both from exogenous and from endogenous sources. Thanks to the activation of DDR, cells can block cell cycle progression, to have time to repair the DNA lesions; alternatively, in presence of irreparable damages, cells are committed to apoptosis or senescence, to prevent the replication of damaged genomes, because mutations could be maintained, leading to genomic instability and predisposition to cancer development. One of the proteins recently found to play an important role in the DDR is DBC1 (deleted in breast cancer 1, CCAR2). In particular, DBC1 is a substrate of ATMjATR and a biological inhibitor of the deacetylase SIRT1, the main protein involved in p53 deacetylation. DBC1, through its physical interaction with SIRT1, blocks its deacetylase activity, preserving p53 acetylation and activation and promoting p53-dependent apoptosis. The data presented in this thesis further characterize the mechanism through which DBC1 regulates SIRT1, as I found that it co-operates with Chk2 and the proteasome activator REGy to exert this function. Moreover, these studies unravel a novel role for DBC1 in the repair of heterochromatic DNA lesions through the promotion of Chk2 activity towards KAP1, a Chk2 substrate involved in the modulation of chromatin remodelling. In addition, the data obtained with a genome wide expression analysis of cells lacking DBC1 revealed a crosstalk between DBC1 and TSPYL2, a protein that we found to playa crucial role in the modulation of p53 activation and induction of apoptosis, by regulating the activity of SIRTl and p300. Overall, these studies extend the knowledge of DBCl functions in DDR and DNA repair, and report for the first time a novel role for TSPYL2 in the regulation of p53 activation upon DNA lesions.
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Patenauden, Geneviève. "Quantifying forest carbon stocks and changes in support of the Kyoto Protocol." Thesis, University of Oxford, 2006. https://ora.ox.ac.uk/objects/uuid:0d69355d-db71-45a6-b0e7-7f9673f1118b.

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This thesis brings together research conducted on field based, remote sensing and modelling approaches to meet reporting requirements set by the Kyoto Protocol. Parties are given the option to meet part of their greenhouse gases reduction requirements through the conservation and enhancement of the carbon stored in forest ecosystems. Two contrasting forests (Monks Wood, UK, 52°24' N, 0°14' W and Thetford UK, 52°30' N, 0°30' E) were selected for the development and assessment of the selected methods. Field-based measurements were used to quantify carbon stocks in Monks Wood, providing the first exhaustive assessment of the carbon content held in a UK semi-natural woodland. The total carbon content of the stands varied from 346 to 616 tonnes per hectare (t ha-1) and highlighted the importance of broadleaved woodlands as carbon stores in the UK. A quantitative appraisal of remote sensing methods was also provided. For land cover discrimination, both optical and radar remote sensing have been successful. For forest carbon stock estimation, LiDAR approaches may provide the only viable remote sensing tool for this purpose. As a result, a LiDAR-based method was developed and the results compared to field-based estimates. At the stand level, the agreement between the field-based and the LiDAR estimates was r=0.85. At the woodland level, due to the enhanced capability of LiDAR to monitor the natural variability of carbon across the woodland, the estimates were nearly 24% lower than those from the ground. Remote sensing of field-based approaches are unsuitable alone for quantifying below-ground carbon content and can be resource intensive. Process-based models enable an estimation of below-ground components to be made. Much uncertainty however arises from the lack of information available on model parameter values. The 3-PG model was used to simulate forest production in Thetford forest and a Bayesian calibration was applied. The results showed that this statistical approach could provide an overall framework for integrating and quantifying the uncertainty in the combined field based, remote sensing and modelling datasets, a result highly relevant in the context of the Kyoto Protocol.
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Matty, Nazek. "Historical reconstruction of Sennacherib's campaign against Judah and Jerusalem in 701 B.C." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:52c94dd4-db51-4af0-88bc-5b6f9940af34.

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This thesis has attempted a reconstruction of Sennacherib’s campaign against Judah in 701. The purpose of this resconstruction has not been to reach a definitive picture of the events of 701 but rather to come to the best possible hypothesis based upon a wide study of the relevant texts. The best historical hypothesis concerning what happened in 701 must attempt to give equal weight to each piece of evidence in each relevant area, whether literary or archaeological. My justification for returning to this much-discussed area therefore is that previous scholarship has failed to meet this criterion for giving the best historical hypothesis. Over the course of my investigation I examined the relevant Assyrian inscriptions, not merely those relating to the third campaign, and the purported instances of biblical evidence, as well as engaging with archaeological and literary considerations. I showed that the most important theories offered up to this point each contradict or contend with an important piece of contrary evidence. Then, I suggested a view of my own which is, as far as possible, commensurate with all the evidence available.
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Raynes, Rachel Rene. "SIRT1 Regulation of the Heat Shock Response in an HSF1-Dependent Manner and the Impact of Caloric Restriction." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4567.

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The heat shock response (HSR) is the cell's molecular reaction to protein damaging stress and is critical in the management of denatured proteins. Activation of HSF1, the master transcriptional regulator of the HSR, results in the induction of molecular chaperones called heat shock proteins (HSPs). Transcription of hsp genes is promoted by the hyperphosphorylation of HSF1, while the attenuation of the HSR is regulated by a dual mechanism involving negative feedback inhibition from HSPs and acetylation at a critical lysine residue within the DNA binding domain of HSF1, which results in a loss of affinity for DNA. SIRT1 is a NAD+-dependent histone deacetylase that has been reported to deacetylate HSF1, thus promoting stress-induced HSF1 DNA binding ability and increasing HSP expression (Westerheide, Anckar et al. 2009). While an abundance of research is aimed to investigate SIRT1 substrate regulation, the mechanism in which SIRT1 itself is regulated is less understood (Haigis and Sinclair 2010). Positive and negative modulators of SIRT1 include AROS and DBC1, respectively, and have yet to be investigated in relation to SIRT1-dependent regulation of the HSR. In addition, metabolic stress such as caloric restriction has been shown to modulate SIRT1 activity in yeast (Rahat, Maoz et al. 2011), but the effect of caloric restriction on the HSR is unknown. Using cell-based assays, we have investigated how the HSR may be controlled by factors influencing SIRT1 activity. We found that heat shock results in an increase in the cellular NAD+/NADH ratio and an increase in recruitment of SIRT1 to the hsp70 promoter. Furthermore, we found that the SIRT1 modulators, AROS and DBC1, impact hsp70 transcription, HSF1 acetylation status, and HSF1 recruitment to the hsp70 promoter. The nematode Caenorhabditis elegans is a useful model organism for testing the relationship between the HSR and metabolism, as these animals can easily be calorically-restricted via bacterial limitation and possess the mammalian SIRT1 homolog, Sir2.1. Using C. elegans, we demonstrate that caloric restriction and heat shock have a synergistic effect on the HSR in a sir2.1-dependent manner. We show that caloric restriction increases the ability of heat shock to promote thermotolerance and fitness in wild-type animals and to preserve movement in a polyglutamine toxicity neurodegenerative disease model and that this effect is dependent on sir2.1. These studies provide insight into SIRT1-dependent regulation of the HSR and the impact of metabolism on this response. We highlight the SIRT1 modulators AROS and DBC1 as two new targets available for therapeutic regulation of the HSR and add caloric restriction as another HSR activator that can synergize with heat shock.
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De, Angelis Annalisa. "Electro-optical pump-probe system suitable for the investigation of electroporated biological cells." Limoges, 2012. http://aurore.unilim.fr/theses/nxfile/default/46acb249-db11-4e5f-a29e-8bfcec5a48f4/blobholder:0/2012LIMO4016.pdf.

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A sufficiently strong electric field is able to change the cell membrane permeability, forming aqueous pores across it, hence the name electroporation, permitting the passage, otherwise forbidden, of ions and molecules. Since its efficient application in biotechnology and medicine (e. G. Electrochemotherapy), ms/μs-pulse-induced electroporation draws growing interest. Recently, the application of nanosecond pulses has showed electroperturbation on intracellular membranes, opening the way to subcellular manipulations. To date, the mechanisms beyond the electroporation are not still well known. The lack of ultra-rapid and flexible pulsers for cell stimulation on the one hand, and the rapid and subcellular-scale involved dynamics on the other hand, make the investigations complex. In this context, we have designed and realized a compact system providing both the electric pump and the optical probe for electroporation studies. The electric pump consists of a photocommutation-based pulse generator triggered by a sub-nanosecond microchip laser that also provides the optical excitation of the multiplex-CARS microscope used for cell imaging. The main innovation of this system is represented by the sub-nanosecond regime of the common laser source. This choice is justified by the need for synchronizing the nanosecond electrical stimulation with the optical detection. A detailed analysis in the time and frequency domains has been performed in order to verify the whole system efficiency and applicability to nano-electroporation investigations
Un champ électrique suffisamment intense induit des effets sur la membrane cellulaire, notamment la formation des pores qui permettent le passage , autrement interdit, de ions et molécules, d’où le nom électroporation. Grâce à son application à la biotechnologie et à la médecine (électrochimiothérapie), l’électroporation représente un phénomène de grand intérêt. Récemment, des impulsions de l’ordre de la nanoseconde ont étés appliquées, montrant des effets sur les membranes intracellulaires. Les mécanismes qui sont à la base de l’électroporation ne sont pas encore complètement compris. D’une part, il n’y a pas en commerce de générateurs ultra-rapides et flexibles pour une stimulation électrique adaptée. D’autre part, la détection de phénomènes à l’échelle subcellulaire et de dynamiques temporelles rapides résulte très difficile. En ce contexte, nous avons conçu et réalisé un système électro-optique pompe-sonde. Il se compose d’un système optoélectronique dédié à la génération d’impulsions ultracourtes et de forte intensité, et d’une source pour l’imagerie optique non linéaire basée sur la microspectroscopie multiplex-CARS. Les deux sources sont déclenchées par le même laser fonctionnant en régime sub-nanoseconde. Ce régime temporel permet une synchronisation efficace des deux systèmes, mais il nécessite d’une étude approfondie des effets optiques non linéaires qui induisent l’élargissement spectral du faisceau, indispensable pour l’imagerie multiplex-CARS. Une caractérisation dans le temps et en fréquence a été menée afin de vérifier les performances du system entier et son emploi aux études de nano-électroporation
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Callow, Nichola. "The cognitive and motivational effects of imagery on sport performance." Thesis, Bangor University, 2000. https://research.bangor.ac.uk/portal/en/theses/the-cognitive-and-motivational-effects-of-imagery-on-sport-performance(4ea1fa97-db21-467c-a917-84a5b7fa9d7b).html.

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This thesis is written as a collection of research papers through which the cognitive and motivational effects of imagery on sports performance were investigated. A number of research methodologies, ranging from a quasi-experimental design to a multiple-baseline across participants design, were employed to explore the effects of imagery. The first section of this thesis explored the cognitive effects of imagery. Specifically, study I examined the effects of different visual imagery perspectives and kinaesthetic imagery on the acquisition and retention of a simple gymnastics routine. External visual imagery was shown to have superior effects over internal visual imagery for this form-based task. A significant interaction was found in the retention phase; however, follow up tests failed to clarify the nature of the interaction. Study 2 and study 3 further investigated the imagery perspective issue by exploring the strength of relationship between external visual imagery and kinaesthetic imagery, and between internal visual imagery and kinaestlictic imagery. Results indicated that when the participant is the object of the image, kinaesthetic imagery has a greater association with external visual imagery than with internal visual imagery. However, because the tasks that participants imaged were essentially form-based, the results may not generalise to other types of tasks. The second section of the thesis examined the motivational effects of imagery. Study 4 employed a multiple-baseline across participants design to establish the effect of a mastery imagery intervention on sport confidence. Consistent with Paivio's (1985) proposals, the results suggested that imagery has a motivational function as the imagery intervention was found to increase confidence. Study 5 further considered the imagery confidence relationship and two factors which may moderate this relationship, that is skill level and sport-type. The results suggest that in team sport players the type of imagery associated with confidence depends on the skill level of the player.
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Li, Pengcheng. "Functional analysis of SOX3 binding at the Dbx1 locus." Thesis, 2014. http://hdl.handle.net/2440/85196.

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Sox3 a members of the SOX transcription factor family, is essential for normal brain development and required for growth of pituitary and hypothalamus. Sox3, as well as Sox2 which is another member in SOXB1 subfamily are widely expressed in neural progenitor cells and show functional redundancy. ChIP-seq data by Bergsland et al, 2011 has identified five putative SOX3 binding sites near/at the Dbx1 locus. Microarray data from the lab (N. Rogers, unpublished data) has identified Dbx1 as downregulated in Sox3 null neural progenitor cells. Together these data suggest that Dbx1 may be regulated directly by SOX3. To investigate the possibility that SOX3 regulates the Dbx1 locus in vitro, we performed gel shift assays and Luciferase Reporter Assays to see if SOX3 binds any of the five Dbx1 regulatory sites. Due to time constraints we were not able to optimize the gel shift assays to obtain any informative results. Secondly, we optimized Luciferase Reporter Assays providing preliminary data suggesting SOX3 may bind at one of the tested Dbx1 sites. To study the redundancy between Sox2 and Sox3, Sox2 was also tested in the Luciferase Reporter Assays indicating Sox2 may also regulate the same site as Sox3 . Due to time constraints, the other three binding sites remain to be analyzed in the future. The function of Dbx1 is best characterized in the context of the developing neural tube (also known as the spinal cord). To identify how other neural tube marker genes are regulated by Sox3, qPCR was performed with some marker genes in Sox3 null E9.5 mouse embryos compared with WT embryos. Dbx1, Pax6, Ngn2 and Olig2 all showed significant decrease in Sox3 null. Further study of these genes will be required to assess the significant outcome of their down regulation in an in vivo context.
Thesis (M.Phil.) -- University of Adelaide, School of Molecular and Biomedical Science, 2014
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Fiala, Tomas. "Polymer supported probes and drugs for targeted brain imaging and pharmacology." Thesis, 2020. https://doi.org/10.7916/d8-dbv1-gp60.

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This doctoral thesis details a series of projects at the border of chemistry and neuroscience leading to the development of a novel family of probes which chemically target specific cells and molecules in the brain. Chapter 1 concisely introduces the history, development and applications of probes for monitoring brain activity and highlights synthetic voltage sensitive dyes as probes which have not yet reached their full potential, partly due to the lack of targeting strategies in brain tissue. Chapter 2 details the development of a new class of polymer-supported probes for ligand-directed delivery of fluorescent voltage sensitive dyes to monoaminergic neurons in live brain tissue. The polysaccharide dextran equipped with dichloropane as a ligand and either an electrochromic or PeT-based voltage sensor selectively targets dopaminergic and noradrenergic axons in mouse brain slice preparations. The new probes enabled voltage imaging in a defined neuronal population without the use of genetic manipulation. All following chapters describe modification of one of the components of the targeting platform developed in Chapter 2 aiming to optimize its performance or broaden its application potential. Chapter 3 extends the developed polymer platform to the targeting of a different molecular target – the AMPA-type glutamate receptor – via a ligand-directed covalent labeling strategy. Chapter 4 examines PEG as an alternative polymer carrier and shows that while dextran is more universal as a carrier, PEG provides superior targeting selectivity with negatively charged PeT-based voltage sensors. A series of targetable probes with improved voltage sensitivity based on the PEG platform is introduced here as well. Chapter 5 describes the synthesis of targetable probes carrying voltage sensors for imaging modalities other than visible light fluorescence, specifically for short wave infrared (SWIR) fluorescence and photoacoustic (PA) imaging. Chapter 6 shows the first steps towards adapting the delivery platform to the development of dual-ligand drugs for cell-selective pharmacology in the brain.
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18

Gantois, Josephine. "All things plants: An ecosystem view of sustainable development." Thesis, 2021. https://doi.org/10.7916/d8-dbx3-0v07.

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Achieving societal well-being goals is inextricably linked to the preservation of many ecosystem functions. This dissertation adopts a plant lens, to contribute to our understanding of sustainable ecosystem functioning. Specifically, it sheds light on some plant physiology, phenology, and ecology processes, which matter for sustainable development: tree growth response to high temperatures, annual fluctuations in the timing of plant flowering, and ecological benefits of crop diversity that translate into economic returns. In addition, it illustrates how large-scale data proxies can be used to document large scale patterns that arise from individual plant processes. Chapter 1 documents a new methodology for estimating tree-level temperature response curves, using tree ring data and a degree-day framework. It uses those curves to document harmful impacts of high temperatures for tree growth across the US, and shows that there is limited acclimatization, but some adaptation to those high temperatures in a sample of climate sensitive and long-lived trees. Chapter 2 shows that satellite imagery and deep learning tools can be leveraged, to monitor interannual variations in the timing of plant flowering at large scales. It documents the predictive performance of two models: one adapted to monitoring crop flowering, the other adapted to monitoring shifts in the onset of spring flowering. Finally, chapter 3 highlights remaining gaps between empirical evidence of crop diversity benefits, and portrayal of those benefits in economic models of optimal crop diversity choice. Together, these chapters illustrate that bridging scales and disciplines is a difficult task, although it is necessary for understanding the sustainability of the human environmental footprint.
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