Global ETD Search

1	Eternal Return Kopacz, Timothy N. January 2013 (has links) Thesis advisor: John Houchin / The objective of this project was to attempt not only to adapt the novel "The Master and Margarita" by Mikhail Bulgakov to the stage, but rather to translate it in both time and place to the stage. It has been more than 60 years since the novel was written, and as such the concerns of the characters have changed both in time and locale. Not only are their objectives adjusted, but the novel is ultimately that: a novel. Being a theatrical adaptation, the play must acknowledge its own existence as such and take issue with its form as much as "The Master and Margarita" does its own. The play is, ultimately, a failed one in my opinion. The greatest downfall thereof being the fact that theatre, drama, is centered around a single thing: conflict. The devil can be in conflict with no one but the divine, and as such any time he is on stage there is simply something missing. The failure is, to a certain extent, befitting of the piece for what it takes to heart as its issues. Enjoy. / Thesis (BA) — Boston College, 2013. / Submitted to: Boston College. College of Arts and Sciences. / Discipline: College Honors Program. / Discipline: Theater. Bulgakov modernism Master and Margarita adaptation full-length redemption
2	Sickle Fenbert, Abbey 08 April 2016 (has links) Please note: creative writing theses are permanently embargoed in OpenBU. No public access is forecasted for these. To request private access, please click on the locked Download file link and fill out the appropriate web form. / No abstract required. / 2031-01-01 Theater Holodomor Ukraine All-female ensemble Full-length play
3	Isolation and Characterization of Plastidic Glucose-6-Phosphate Dehydrogenase (G6PDH) from Castor (Ricinus communis L.) Law, Ka-Yu 27 September 2007 (has links) Abstract Plant cells contain plastids, organelles dedicated to performing specific biochemical processes including photosynthesis, starch and oil biosynthesis. Fatty acid biosynthesis in oil seeds occurs in one type of plastid termed the leucoplast. Anabolic metabolism in leucoplasts includes the production of fatty acids and amino acids that depend on the availability of reductants such as NADPH. NADPH can be generated in plastid by glucose 6-phosphate dehydrogenase (G6PDH) which is the chief control enzyme and first step in the Oxidative Pentose Phosphate Pathway (OPPP). G6PDH catalyses the reaction of NADP+ and glucose 6-phosphate to NADPH and 6-phosphogluconate. At least two compartment-specific isoforms of G6PDH exist in plants, a cytosolic and a plastidic form. In this study, castor oil seed (COS) (Ricinus communis L.) was used as a model enzyme system for the ongoing study of oil biosynthesis in plants. This is the first ever report of the full-length clone of the plastidic isoform of G6PDH being isolated from a castor cDNA library using polyclonal potato plastidic G6PDH antiserum. The full-length cDNA was sequenced and compared to other G6PDH genes from higher plants, the castor sequence reveals conserved regions and conserved cysteine residues similar to other higher plant G6PDH. Over expression of the recombinant cleaved fusion protein in an E. coli expression system from the isolation of the cDNA clone shows it is enzymatically active, stable and unlike other plastid G6PDH’s dithiothreitol insensitive. In fact this G6PDH shows increased activation in the presence of dithiothreitol. Initial kinetic characteristics shows that it behaves in a similar fashion enzymatically when compared to other higher plant chloroplast G6PDH. The gene sequence and initial kinetic findings for castor G6PDH concur with other higher plant, non-photosynthetic, plastidic isoforms. / Thesis (Master, Biology) -- Queen's University, 2007-09-19 13:41:54.584 Full Length Clone Transit Peptide
4	Structural Analysis of TRPV2 by Cryo-Electron Microscopy Reveals Regulatory Diversity Among the ThermoTRPV Channels Huynh, Kevin Weijian 13 September 2016 (has links) No description available. Biology Biochemistry
5	A transcriptome analysis of apple (Malus x domestica Borkh.) cv ‘golden delicious’ fruit during fruit growth and development Chikwambi, Zedias January 2013 (has links) Philosophiae Doctor - PhD / The growth and development of apple (Malus x domestica Borkh.) fruit occurs over a period of about 150 days after anthesis to full ripeness. During this period morphological and physiological changes occur defining fruit quality. These changes are a result of spatial and temporal patterns of gene expression during fruit development as regulated by environmental, genetic and environmental-by-genetic factors. A number of previous studies partially characterised the transcriptomes of apple leaf, fruit pulp, whole fruit, and peel plus pulp tissues, using cDNA micro arrays and other PCR based technologies. These studies, however, remain limited in throughput and specificity for transcripts of low abundance. Hence, the aim of this project was to apply a high throughput technique to characterise the full mRNA transcriptome of the ‘Golden Delicious’ fruit peels and pulp tissues in order to understand the molecular mechanisms underlying the morphophysiological changes that occur during fruit development. Apple fruit Fruit pulp Fruit peel Transcriptome Differential gene expression Full-length transcript reconstruction Fruit development Genomics RNA-seq Bioinformatics
6	The Role of Regulatory Genes in Mediating Growth Arrest by all-trans Retinoic Acid in Ovarian Carcinoma Cell Lines Sirisani, Evelyn January 2012 (has links) All-trans retinoic acid (atRA) mediated growth inhibition results in the arrest of the cell cycle during the G1 phase in CAOV3 cells but not SKOV3 ovarian carcinoma cells. The G1 checkpoint is regulated by a multitude of molecules such as the retinoblastoma family of proteins, cyclins, cyclin dependent kinases (CDKs) and cyclin dependent kinase inhibitors (CDKis). CAOV3 cells, which are atRA sensitive, have been shown to express p16INK4a (p16), a cyclin dependent kinase inhibitor regulating the G1 checkpoint. However, atRA resistant SKOV3 cells do not express p16. In these studies, we investigated the role of p16 in mediating atRA induced growth arrest. Our results show that overexpression of p16 in SKOV3 cells leads to growth inhibition following atRA treatment. However, the inhibition is short-term due to the loss of p16 expression. Nevertheless, these results show that p16 plays a role in atRA mediated growth inhibition in ovarian carcinoma cells and that modulation of p16 expression can determine the growth response to atRA. Additionally, we also examined the effect of atRA treatment on the expression of homeobox genes in the CAOV3 cells and SKOV3 cells model system. Homeobox genes comprise a family of transcription factors which function during embryonic development to control pattern formation, differentiation and proliferation. Besides their dominant role during embryogenesis, they are also expressed in adults. In human tumors, an association between the deregulation of the expression of homeobox genes and oncogenic transformation has been reported. It is known that some homeobox genes are atRA targets due to the presence of retinoic acid response element (RARE) either in their promoter region or in their 3' region. In these studies we examined the expression of 13 homeobox genes in CAOV3 cells and SKOV3 cells following ethanol or atRA treatment. The 13 homeobox genes were analyzed because previous studies done by our laboratory observed differences in expression of these homeobox genes when comparing atRA sensitive oral squamous carcinoma cells (SCC) to atRA resistant oral squamous cell carcinoma cells. Of the 13 homeobox genes analyzed in the ovarian carcinoma cell model system, we found HOXA1 and HOXB4 to be upregulated by atRA in CAOV3 cells but not in SKOV3 cells. We also found that the induction of HOXA1 and HOXB4 mRNA expression in CAOV3 cells occurred as a respond to atRA treatment and is not due to a generalized response because of overall growth reduction. Interestingly, HOXA1 has two alternatively spliced forms. The mRNA expression of the truncated form of HOXA1 is highly induced by atRA when compared to its full length form. HOXB1, which is HOXA1 target gene, was not upregulated following atRA treatment. These results suggest that: 1) expression of p16 plays a role in mediating atRA growth inhibition; 2) HOXA1 and HOXB4 also play a role in mediating growth suppression by atRA; and 3) the truncated form of HOXA1 is induced by atRA treatment and may play a role in mediating growth inhibition by atRA, perhaps by acting in a dominant negative fashion. / Microbiology and Immunology Microbiology Immunology Biology, Molecular All-trans Retinoic Acid Full Length Hoxa1 Hoxa1 Hoxb4 P16ink4a Truncated Form Hoxa1
7	Structure, Stability and Evolution of Multi-Domain Proteins Bhaskara, Ramachandra M January 2013 (has links) (PDF) Analyses of protein sequences from diverse genomes have revealed the ubiquitous nature of multi-domain proteins. They form up to 70% of proteomes of most eukaryotic organisms. Yet, our understanding of protein structure, folding and evolution has been dominated by extensive studies on single-domain proteins. We provide quantitative treatment and proof for prevailing intuitive ideas on the strategies employed by nature to stabilize otherwise unstable domains. We find that domains incapable of independent stability are stabilized by favourable interactions with tethered domains in the multi-domain context. Natural variations (nsSNPs) at these sites alter communication between domains and affect stability leading to disease manifestation. We emphasize this by using explicit all-atom molecular dynamics simulations to study the interface nsSNPs of human Glutathione S-transferase omega 1. We show that domain-domain interface interactions constrain inter-domain geometry (IDG) which is evolutionarily well conserved. The inter-domain linkers modulate the interactions by varying their lengths, conformations and local structure, thereby affecting the overall IDG. These findings led to the development of a method to predict interfacial residues in multi-domain proteins based on difference evolutionary information extracted from at least two diverse domain architectures (single and multi-domain). Our predictions are highly accurate (∼85%) and specific (∼95%). Using predicted residues to constrain domain–domain interaction, rigid-body docking was able to provide us with accurate full-length protein structures with correct orientation of domains. Further, we developed and employed an alignment-free approach based on local amino-acid fragment matching to compare sequences of multi-domain proteins. This is especially effective in the absence of proper alignments, which is usually the case for multi-domain proteins. Using this, we were able to recreate the existing Hanks and Hunter classification scheme for protein kinases. We also showed functional relationships among Immunoglobulin sequences. The clusters obtained were functionally distinct and also showed unique domain-architectures. Our analysis provides guidelines toward rational protein and interaction design which have attractive applications in obtaining stable fragments and domain constructs essential for structural studies by crystallography and NMR. These studies enable a deeper understanding of rapport of protein domains in the multi-domain context. Protein Sequence Protein Structure Multi-Domain Proteins GSTO-1 Full-length Proteins Multi-Domain Proteins - Evolution Multi-Domain Proteins - Folding Human Glutathione S-Transferase Omega-1 Multi-Domain Proteins - 3D Modelling Protein Folding Proteins - Stability Amino Acid Sequence Single Nucleotide Polymophisms (SNPs) Homologous Protein Structures Biochemistry
8	The Effects of Immune Regulation and Dysregulation: Helper T Cell Receptor Affinity, Systemic Lupus Erythematosus and Cancer Risk, and Vaccine Hesitancy Johnson, Deborah K. 03 June 2020 (has links) Helper T cells direct the immunological response to foreign pathogens and cancer. To become activated, helper T cells must recognize unique peptides presented on major histocompatibility complex II (pMHCII) by antigen presenting cells (APCs) with their T cell receptor (TCR). While much is known about helper T cell activation signaling cascades and the subsequent roles of helper T cell subsets, the initiation of helper T cell activation by the TCR and other co-receptors is less well understood. Specifically, the affinity of the TCR for its pMHCII can change helper T cell subset fate, proliferation, and alter the risk for activation induced cell death. High affinity TCRs are attractive targets for immunotherapies, but little is known about how helper T cells respond to high affinity TCRs. Here we describe high affinity TCR activation thresholds for both full length TCRs and chimeric antigen receptor TCRs both with and without the presence of the coreceptor CD4 and propose a mechanism whereby CD4 inhibits T cell activation via Lck sequestration and a CD4-independent method. Dysregulated helper T cells play critical roles in the development and perpetuation of systemic lupus erythematosus (SLE), a systemic autoimmune disease that causes widespread inflammation and organ damage throughout the body. Chronic inflammation in SLE affects the immune response to viruses and the risk of developing cancer. However, in SLE patients, it is unclear if viruses initiate the development of cancer directly or if the effects are non-interacting and concomitant. Here we describe the interactions between SLE, viruses, and cancer risk revealing that viruses and SLE do interact to increase the both the overall cancer risk and the risk for hematological malignancies. Due to vaccine efficacy, vaccine preventable diseases (VPDs) are no longer commonly experienced or understood by the public. Vaccines are a victim of their own success and according to the World Health Organization (WHO), vaccine hesitancy (VH) is one of the top threats to global health. VH is the refusal to accept vaccinations and the reasons for VH vary across time, place, and vaccine. Refuting VH is difficult as directly confronting false assumptions can cause individuals to become more entrenched in their position resulting in confirmation bias. Adults with VH attitudes are often motivated by concerns over personal liberty, harm, independence, and body purity. Here we describe the results of a VPD interview- and education-based intervention geared towards promoting positive vaccine attitudes for young adults and demonstrate that education focused on VPDs is more effective than vaccine safety. Helper T cell CD4+ T cell CD4 T cell receptor (TCR) Lck IL-2 T cell activation TCR single chain signaling (TCR-SCS) chimeric antigen receptor (CAR) full length TCR (flTCR) high affinity TCRs systemic lupus erythematosus (SLE) cancer-risk viruses vaccine hesitancy (VH) vaccine preventable diseases (VPDs) vaccines Life Sciences
9	Caractérisation génotypique des réservoirs viraux qui persistent chez les personnes vivant avec le VIH sous traitement antirétroviral Dufour, Caroline 05 1900 (has links) Les personnes qui vivent avec le VIH (PVVIH) doivent prendre un traitement d’antirétroviraux combinés (ART) pour contrôler la réplication virale et empêcher le développement d’une immunodéficience dont l’issue est fatale. Les ART protègent les cellules saines de l’infection et permettent ainsi de rendre la charge virale plasmatique indétectable. Cependant, l’arrêt des ART entraine presque inévitablement un rebond de la charge virale, puisque le virus n’est jamais complètement éliminé par le système immunitaire. En effet, de multiples cellules infectées, où le virus s’est intégré et demeure dans un état de latence, restent présentes tout au long de la vie des PVVIH. Une partie de ces cellules infectées forme le réservoir compétent pour la réplication. Les provirus responsables du rebond de la charge virale possèdent trois caractéristiques : ils gardent la capacité d’être réactivés (sortie de latence), ils sont génétiquement intacts, et ils peuvent produire de nouvelles particules virales infectieuses. Afin de guérir les PVVIH de l’infection, il faut donc cibler les quelques rares cellules portant un provirus intact et inductible. Pour ce faire, il est impératif de comprendre comment ces cellules sont maintenues pendant les années de ART, de les localiser dans tout l’organisme, et d’identifier ce qui peut les distinguer des autres. Ce sont ces trois aspects que nous avons abordés au cours des travaux de recherche présentés dans cette thèse, autant à l’échelle de la cellule unique que de l’organisme entier. Nos résultats montrent que les provirus compétents pour la réplication persistent dans des lymphocytes T CD4+ mémoires exprimant l’intégrine VLA-4 en grande quantité, que les provirus intacts peuvent subsister au sein de différents compartiments anatomiques, que les provirus inductibles et compétents pour la traduction de la protéine virale p24 sont majoritairement défectifs, et que l’expansion clonale est un mécanisme important qui favorise le maintien du réservoir viral dans le sang et dans les tissus tout en favorisant la diversité phénotypique de ces cellules. / People with HIV (PWH) must take combinational antiretroviral therapy (ART) to control viral replication and avoid developing fatal immunodeficiency. ART allows achieving undetectable plasma viral load, and thus protects uninfected cells from HIV. However, ART interruption will almost inevitably result in a viral rebound since HIV is never completely cleared by the immune system. Indeed, a group of infected cells, where the virus has integrated and remains in a latent state, persists throughout the life course of PWH, and some of these cells form the replicationcompetent reservoir. Proviruses responsible for viral rebound have three characteristics: they can be induced to exit their latent state, they are genetically intact, and they are able to produce new infectious viral particles. Therefore, in order to cure PWH, it is essential to target the few cells with intact and inducible provirus, and to be able to do so, it is imperative to understand how these cells are maintained during years of ART, to localize them throughout the body, and to identify what distinguishes them from other cells. These three aspects are the focus of the work presented in this thesis, whether at the single-cell level or looking through the whole body. Our results show that replication-competent proviruses persist in memory CD4+ T cells expressing high levels of the integrin VLA-4, that intact proviruses can persist among various anatomical compartments, that inducible and translation-competent proviruses are predominantly defective, and that clonal expansion is an important mechanism that favors the maintenance of reservoir cells both in the blood and in deep tissues in addition to diversify phenotypically those cells. Réservoir VIH Latence Séquençage quasi complet Phénotype VLA-4 HIV-Flow Expansion clonale Inductibilité Réservoirs anatomiques Compartimentalisation Post mortem Autopsies HIV Latency Near full-length sequencing Phenotype Clonal expansion Inducibility Replication-competent reservoir Anatomical reservoirs Compartmentalization Postmortem Virology / Virologie (UMI : 0720)
10	Micro RNA-Mediated regulation of the full-length and truncated isoforms of human neurotrophic tyrosine kinase receptor type 3 (NTRK 3) Guidi, Mònica 13 January 2009 (has links) Neurotrophins and their receptors are key molecules in the development of thenervous system. Neurotrophin-3 binds preferentially to its high-affinity receptorNTRK3, which exists in two major isoforms in humans, the full-length kinaseactiveform (150 kDa) and a truncated non-catalytic form (50 kDa). The twovariants show different 3'UTR regions, indicating that they might be differentiallyregulated at the post-transcriptional level. In this work we explore howmicroRNAs take part in the regulation of full-length and truncated NTRK3,demonstrating that the two isoforms are targeted by different sets of microRNAs.We analyze the physiological consequences of the overexpression of some of theregulating microRNAs in human neuroblastoma cells. Finally, we providepreliminary evidence for a possible involvement of miR-124 - a microRNA with noputative target site in either NTRK3 isoform - in the control of the alternativespicing of NTRK3 through the downregulation of the splicing repressor PTBP1. / Las neurotrofinas y sus receptores constituyen una familia de factores crucialespara el desarrollo del sistema nervioso. La neurotrofina 3 ejerce su funciónprincipalmente a través de una unión de gran afinidad al receptor NTRK3, del cualse conocen dos isoformas principales, una larga de 150KDa con actividad de tipotirosina kinasa y una truncada de 50KDa sin dicha actividad. Estas dos isoformasno comparten la misma región 3'UTR, lo que sugiere la existencia de unaregulación postranscripcional diferente. En el presente trabajo se ha exploradocomo los microRNAs intervienen en la regulación de NTRK3, demostrando que lasdos isoformas son reguladas por diferentes miRNAs. Se han analizado lasconsecuencias fisiológicas de la sobrexpresión de dichos microRNAs utilizandocélulas de neuroblastoma. Finalmente, se ha estudiado la posible implicación delmicroRNA miR-124 en el control del splicing alternativo de NTRK3 a través de laregulación de represor de splicing PTBP1. RISC complex retinoic acid renilla luciferase real-time quantitative PCR PTBP1 pri-miRNA pre-miRNA post-transcriptional regulation piRNA PicTar pGL4.13 PCR P-body p75NTR overexpression NTRK3 NTRK2 NTRK1 non-coding RNAs NGF neurotrophin neurotrophic signaling neuronal differentiation neurodevelopment neuroblastoma nervous system mRNA miRNA target prediction miRNA profiling miRNA mimic miRNA microarray miRNA inhibitor miRanda microRNA microarray luciferase assay Ingenuity Pathway Analysis (IPA) heLa cells gene silencing gene regulation full-length isoform (FL-NTRK3) firefly luciferase ERK disease dicer cancer development BDNF argonaute alternative splicing 3'UTR RNAhybrid RT-PCR SH-SY5Y cells siRNA standard error synaptic plasticity target validation TargetScan transfection translational repression TrkA TrkB TrkC truncated isoform (TR-NTRK3) tyrosine kinase (TK) western blot 575 61

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