Дисертації з теми "Cell division and cell death"
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Cheng, Jade. "Regulation of cell division and cell death by GRASP65." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544414.
Повний текст джерелаOtake, Andreia Hanada. ""Papel de dissialogangliosídios na proliferação e morte celular induzida de melanócitos e melanomas in vitro"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26052006-113740/.
Повний текст джерелаDisialoganglioside GD3 and its derivatives are melanoma progression markers. To evaluate the possible roles of these molecules along melanoma progression, we have transfected the GD3 synthase gene (ST8Sia I) in a melanocyte cell line. Accumulation of GD3 did not confer any proliferative advantage to melanocytes. However, GD3 expression was associated with cell survival. The autonomic growth of melanomas is in part related to a constitutive activation of fibroblast growth factor dependent pathways. GD3 expression did not alter the proliferative response to either FGF-1 or FGF-2. However, GD3 and other membrane glycospingolipids modulate the motogenic activity of FGF-2. GD3 expression sensitizes melanocytes to chemotherapeutic agent-induced cell death, as cisplatin and vimblastin. On the other hand, GD3 turned melanocytes more resistant to temozolomide. Chemosensitization to vimblastin, but not to the other drugs, was dependent on the presence of GD3 within the cells, as shown by metabolic depletion of glycosphingolipids
Chalabi, Asma. "Processus d'analyse dynamique pour l'imagerie de cellules vivantes permettant la détection des réponses cellulaires aux anticancéreux, par traitement de l'image et du signal et apprentissage automatique profond." Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6004.
Повний текст джерелаCell division and cell death are the main indicators to evaluate cancer drug action, and only their accurate measures can reveal the actual potency and efficacy of a compound. The detection of cell division and cell death events in live-cell assays has the potential to produce robust metrics of drug pharmacodynamics and return a more comprehensive understanding of tumor cells responses to cancer therapeutic combinations. Knowing precisely when a cell death or a cell division occurs in a live-cell experiment allows to study the relative contribution of different drug effects -such as cytotoxic or cytostatic effects, on a cell population. Yet, classical methods require dyes to measure cell viability as an end-point assay with whole population counts, where the proliferation rates can only be estimated when both viable and dead cells are labeled simultaneously.Live-cell imaging is a promising cell-based assay to determine drug efficacies, with the main limitation being the accuracy and depth of the analyses to detect and predict automatically cellular response phenotypes (cell death and division, which share some morphological features).This thesis introduces a method integrating deep learning using neural networks, and image and signal processing to perform dynamic image analyses of single-cell events in time-lapse microscopy experiments of drug pharmacological profiling. This method works by automatically tracking the cells, extracting radiometric and morphologic cell features, and analyzing the temporal evolution of these features for each cell so as to detect cellular events such as division and cell death, as well as acquiring signaling pathway dynamics.A case of study comprising the analyses of caspase-8 single-cell dynamics and other cell responses to cancer drugs is presented. The aim is to achieve automatically, at a large scale the necessary analyses to augment the phenotype prediction method available in the lab (Fateseq) and to apply it to various cancer cell lines of a human cancer cell line panel to improve our live-cell OMICS profiling approaches, and, in a longer term, to scale up pharmacological screening of new cancer drugs
Green, Katherine J. "The effect of acute exercise on T-lymphocyte function." Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/36777/1/36777_Digitised%20Thesis.pdf.
Повний текст джерелаPat, Sze Wa. "Cell metabolism in cell death and cell growth." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.
Повний текст джерелаDix, Christina Lyn. "Adhesion-dependent cell division." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044469/.
Повний текст джерелаEllison, David William. "Cell proliferation, cell death, and differentiation in gliomas." Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295912.
Повний текст джерелаCrisby, Milita. "Cell death in atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.
Повний текст джерелаGorak-Stolinska, Patricia. "Activation induced cell death in human T cell subsets." Thesis, King's College London (University of London), 2002. http://kclpure.kcl.ac.uk/portal/en/theses/activation-induced-cell-death-in-human-t-cell-subsets(eb708e24-eccb-42fc-8930-d62ddf6794c1).html.
Повний текст джерелаRUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.
Повний текст джерелаSkoog, Karl. "Cell division in Escherichia coli." Doctoral thesis, Stockholms universitet, Institutionen för biokemi och biofysik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-62908.
Повний текст джерелаAt the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Submitted. Paper 4: Manuscript.
Uppington, Kay Marie. "Cell death in prion disease." Thesis, University of Bath, 2008. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488879.
Повний текст джерелаWongchaowart, Michael B. "Optimization of cell adhesion environments for a liver cell bioreactor." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/34156.
Повний текст джерелаIncludes bibliographical references (p. 40-44).
The MilliF bioreactor offers great potential for the formation of i vivo-like liver tissue outside the body, making it a valuable tool for applications such as drug toxicity models and biosensors. Cell adhesion is an important factor in the maintenance of differentiated hepatocyte functions. Hepatocyte adhesion environments were examined in two settings: spheroid culture prior to seeding in the bioreactor and 2D surface culture methods that could be applied to the bioreactor scaffold. Spheroids were formed either by culturing in spinning suspension or on a static, non-adherent surface. In spheroid culture, the addition of extracellular matrix (ECM) signaling through the use of soluble Matrigel or adhesion protein-coated microspheres did not improve hepatocyte viability or function as assessed by liver-specific gene expression. These results suggest the importance of cell-cell rather than cell-surface interactions in maintaining hepatocytes. Optimal culturing of spheroids in spinning suspension without the ECM addition was found to be 3 days without media changes. 2D surfaces were treated with an adhesion peptide-conjugated comb polymer, preventing nonspecific cell adhesion and allowing attachment through the [alpha]₅[beta]₁ integrin.
(cont.) Varying the proportion of adhesion peptide presented to cells was found to regulate hepatocyte morphology and function; a surface with decreased hepatocyte spreading and liver-specific gene expression closer to in vivo was characterized. Immunoblotting for activated focal adhesion kinase (FAK) revealed that FAK signaling was not induced by attachment to the comb polymer surfaces. Immunostaining for other liver cell types demonstrated that the surface allowed hepatic stellate cell and Kupffer cell adhesion.
by Michael B. Wongchaowart.
M.Eng.
Rabodzey, Aleksandr. "Flow-induced mechanotransduction in cell-cell junctions of endothelial cells." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/41586.
Повний текст джерелаIncludes bibliographical references (leaves 86-92).
Endothelial cells show an unexpected behavior shortly after the onset of laminar flow: their crawling speed decreases ~40% within the first 30 min, but only in a confluent monolayer of endothelial cells, not in subconfluent cultures, where cell-cell interactions are limited. This led us to study early shear effects on cell-cell adherens junctions. We found a 30±6% increase in the number of VE-cadherin molecules in the junctions. The strength of interactions of endothelial cells with surfaces coated with recombinant VE-cadherin protein also increased after laminar flow. These observations suggest that endothelial cell junction proteins respond to flow onset. The process of clustering may induce diffusion of monomers to the junction area, resulting in an overall increase in VE-cadherins in the junctions. To directly confirm the role of adherens junctions in the decrease in cell crawling speed, we used siRNA-knockdown technique to produce cells lacking VE-cadherin. These cells showed no decline in crawling speed under flow. Our interpretation is consistent with previous data on junction disassembly 8 hr after flow onset. The speed of endothelial cell crawling returns to the original level by that time, and junctional disassembly may explain that phenomenon. In order to understand better the change in VE-cadherin distribution under flow and during junction formation and remodelling, we developed a mathematical model of VE-cadherin redistribution in endothelial cells. This model allowed us to develop a quantitative framework for analysis of VE-cadherin redistribution and estimate the amount of protein in the junctions and on the apical surface. In addition to that, the model explains rapid junction disassembly in the leukocyte transmigration and junction formation in subconfluent cells.
(cont.) These studies show that intercellular adhesion molecules are important in the force transmission and shear stress response. Their role, however, is not limited to flow mechanotransduction. Intercellular force transmission has an important application - organ development and, specifically, angiogenesis. We studied the role of VE-cadherin in vessel development in HUVECs and showed that VE-cadherin-null cells do not form vessels in the in vitro assay. This observation confirms the important role of intercellular force transmission in response to external force caused by flow or exerted by other cells.
by Aleksandr Rabodzey.
Ph.D.
Jahnke, Ulrike. "Cell cycle de-regulation and cell death in leukaemia chemotherapy." Thesis, Queen Mary, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439424.
Повний текст джерелаWatson, Andrea. "Heat shock proteins in leukaemia cell differentiation and cell death." Thesis, Aston University, 1990. http://publications.aston.ac.uk/12533/.
Повний текст джерелаSciacovelli, Marco. "Cell death regulation by mitochondrial chaperones in tumor cell models." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421645.
Повний текст джерелаLe cellule tumorali sono caratterizzate dalla capacità di evadere il normale signale apoptotico, così come mostrano una iper-attivazione costitutiva delle vie di signale kinasico. L’integrazione degli stimoli di sopravvivenza e morte si concentra nei mitocondri, dove molti di questi segnali convergono nella regolazione di un canale chiamato poro della transizione di permeabilità (PTP). L’apertura del PTP porta le cellule alla morte ed è regolata da una varietà di fattori e fra questi gli chaperoni giocano un ruolo fondamentale. Nel mio lavoro di tesi ho studiato come gli chaperoni mitochondriali si integrano nelle vie di trasduzione del segnale , modulando il PTP e più in generale la bioenergetica mitocondriale e come questi network regolatori controllano la vitalità cellualre. Nella prima parte del mio lavoro ho studiato una possibile connessione fra la via del segnale Ras/ERK, la cui attivazione costitutiva caratterizza molti tumori favorendo la loro crescita e sopravvivenza, e la ciclofilina D (CyP-D), uno chaperone mitocondriale che regola il PTP. Una frazione di ERK attivo è stato trovato nei mitocondri delle cellule RWPE-2, ottenute tramite trasformazione con v-ki-Ras a partire da cellule dell’epitelio prostatico RWPE-1; in cellule metastatiche di tumore prostatico DU145; e in cellule di osteosarcoma SAOS-2. Tutte queste cellule tumorali mostrano una marcata resistenza alla morte indotta da stimoli pro-apoptotici come l’acido arachidonico e il BH3 mimetico EM20-25, i quali inducono la morte cellulare attraverso il PTP mitocondriale. L’inibizione del PTP e la conseguente resistenza alla morte cellulare indotta da acido arachidonico o EM-20-25 può essere abolita dall’inibizione di ERK con il farmaco PD98059 o con un peptide selettivo inibitorio di ERK. L’inibizione di ERK aumenta la fosforilazione GSK-3 dipendente della CyP-D, mentre l’inibizione di GSK3 protegge dall’apertura del poro. Ne ERK attivo nei mitocondri, ne desensibilizzazione del poro è stata osservata in cellule non trasformate RWPE-1. In conclusione, nelle cellule tumorali l’attivazione dell’ERK mitocondriale desensibilizza il PTP attraverso un asse di segnale che coinvolge GSK3 e Cyp-D. Nella seconda parte del mio lavoro di tesi, ho studiato l’attività di un secondo chaperone mitocondriale, TRAP1/HSP75, fortemente espresso nelle cellule tumorali e che è stato proposto essere coinvolto nella regolazione del poro. Ho dimostrato che TRAP1 interagisce con la CyP-D ed ho caratterizzato la sua funzione di pro-sopravvivenza nei confronti di un vasto spettro di stimoli di morte, incluso lo stress ossidativo, la diamide, il TNFα, e la deplezione di glucosio. Inoltre ho trovato che il knocking-down dei livelli di espressione di TRAP1 attraverso la tecnica dell’RNA interference in cellule di osteosarcoma SAOS-2 facilita l’apertura del PTP, abbassando la soglia per portare le cellule alla morte. TRAP1 modula inoltre il metabolismo cellulare probabilmente la risposta allo stress ossidativo e l’attività della del complesso I della catena respiratoria, con il quale TRAP1 interagisce direttamente sia in cellule che campioni tumorali. La down- regolazione di TRAP1 abolisce il potere tumori genico delle cellule SAOS-2 sia in vitro che in vivo. Tutti insieme questi dati indicano che gli chaperoni mitocondriali come CyP-D e TRAP! Giocano un ruolo importante nella progressione tumorale e costituiscono un possibile target di nuove terapie antineoplastiche.
Cragg, Mark Steven. "Monoclonal antibody induced growth arrest and cell death in B-cell lymphoma cell lines." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242713.
Повний текст джерелаHaddad, F. "Analysis of cell division fidelity of human repair defective cell lines." Thesis, Swansea University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.637194.
Повний текст джерелаJorge, Ana Maria. "Insights into cell wall synthesis and cell division in Staphylococcus aureus." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/8592.
Повний текст джерелаStaphylococcus aureus is a gram-positive bacterial pathogen that besides persistently colonizing healthy individuals, is responsible for a large number of hospital-associated bacterial infections. The extraordinary capacity of S. aureus to acquire resistance to antibiotics led to the emergence of highly resistant strains, mainly methicillin-resistant S. aureus (MRSA) strains, that are a major cause of soft skin and tissue infections and bacteremia. In one third of European countries, including Portugal, more than 25% of S. aureus infections are caused by MRSA strains. The capacity of MRSA strains to resist β-lactam antibiotics (such as penicillin) is mainly due to the acquisition of an extra-species penicillin-binding protein (PBP), PBP2A. PBPs are bacterial enzymes involved in the synthesis of the cell wall polymer peptidoglycan. Besides PBP2A, which is present only in MRSA strains, S. aureus has 4 native PBPs (PBP1-4), which catalyze the polymerization (transglycosylation) and the cross-linking (transpeptidation) of glycan chains, forming a strong yet flexible structure that protects the cell from the high internal osmotic pressure. Peptidoglycan is unique to the bacterial kingdom and its biosynthesis is the target of a vast number of clinically important antibiotics such as β-lactams and glycopeptides. β-lactam antibiotics target the transpeptidase domain of PBPs, halting peptidoglycan synthesis and eventually leading to cell lysis. However, in MRSA strains the existence of PBP2A, which has a low affinity for β-lactams, enables cell wall synthesis to continue even in the presence of these antibiotics. Under these conditions, the transpeptidase domain of PBP2A functionally cooperates with the transglycosylase domain of the unique bifunctional PBP, PBP2, to ensure continued cell wall synthesis and cell survival.(...)
Nestor-Bergmann, Alexander. "Relating cell shape, mechanical stress and cell division in epithelial tissues." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/relating-cell-shape-mechanical-stress-and-cell-division-in-epithelial-tissues(ebf1bce8-ca35-4f5a-8be9-f2e19c96e20d).html.
Повний текст джерелаSpanoudis, Catherine M. "Cell Division Regulation in Staphylococcus aureus." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/7090.
Повний текст джерелаIqbal, Syed Amir. "Asymmetric Cell Division in Mammalian Cells." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503635.
Повний текст джерелаKirby, Melissa Jane. "Regulation of sugar beet cell division." Thesis, De Montfort University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391029.
Повний текст джерелаHarrington, Elizabeth Anne. "Analysis of the molecular regulation of cell proliferation and cell death." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283286.
Повний текст джерелаWeston, Claire Rosemary. "The effects of δMEKK3:ER* on cell death and cell survival". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621377.
Повний текст джерелаWong, Mei Mei. "Effects of Cell Death and Phagocytosis on Mesenchymal Stem Cell Function." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511852.
Повний текст джерелаAbulayha, Abdulmunem M. "Mechanisms of CD20 mediated cell death in B lymphoma cell lines." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403306.
Повний текст джерелаCourtois-Moreau, Charleen Laetitia. "Programmed Cell Death in Xylem Development." Doctoral thesis, Umeå universitet, Umeå Plant Science Centre, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1831.
Повний текст джерелаOron för klimatförändringar och brist på fossila bränslen har ökat påtagligt under de senaste åren. De enorma möjligheter som skogsråvaran erbjuder som alternativ källa för förnyelsebar energi och råmaterial har väckt ett stort intresse också för den biologiska processen bakom vedbildning i träd. Denna avhandling fokuserar på en viktig process i vedbildning: programmerad celldöd (PCD) i xylemet. Xylemcellernas livstid påverkar bildningen av sekundära cellväggar, vilket i sin tur påverkar vedens kvalitativa egenskaperna, så som veddensitet. Trots dess betydelse för viktiga egenskaper hos vedråvaran existerar fortfarande väldigt lite information om xylem PCD på cellulär eller molekylär nivå. I den här avhandlingen belyses de anatomiska, morfologiska och genetiska aspekterna av PCD i xylemutveckling i både stam av hybridasp, Populus tremula (L.) x tremuloides (Michx.) och hypokotyl av det örtartade modellsystemet Arabidopsis thaliana (L. Heynh.). Xylemet i både Populus och Arabidopsis består av två olika celltyper; de vattentransporterade kärlen och de stödjande fibrerna. Det är känt att celldöd i kärlen pågår mycket snabbt efter att den centrala vakuolen brister och de hydrolytiska enzymer släpps in i cytoplasman. I den här avhandlingen ligger fokus på fibrerna i Populus xylemet. Med hjälp av mikroskopianalyser av cellmorfologin (elektronmikroskopi) och DNA-fragmentering i cellkärnan (TUNEL- och Comet-analyser) kunde vi konstatera att till skillnad från kärlen så uppvisar fibrerna en långsam och progressiv nedbrytning av organellerna och cellkärnans DNA före vakuolbristning. Dessutom har kandidatgener för reglering av fibercelldöd identifierats antingen från ett Populus EST bibliotek från vedartade vävnader som genomgår fibercelldöd eller från mikroarray experiment i Populus stam. Dessa kandidatgener är antingen potentiella nya regulatorer av fibercelldöd eller medlemmar av tidigare beskrivna familjer av celldödsrelaterade gener. Bland de sistnämnda finns autofagi-relaterade gener, vilket stöder funktionen av autofagi i samband med autolys av cellinnehållet i xylemfibrerna. Dessa studier pekar därför på en typ av PCD som har inte tidigare beskrivits för xylemet. Arabidopsis är ett alternativt växtmodellsystem för studier av vissa aspekter av vedbildningen, såsom karakteriseringen av negativa regulatorer av PCD. Därför har också hypokotylanatomin analyserats, och ACAULIS5 (ACL5) genen, som kodar för ett enzym i biosyntesen av polyaminer, har visats vara en viktig regulator av xylemspecifikation genom dess negativa effekt på kärlens celldöd. Sammantaget visar denna avhandling att PCD i xylemutvecklingen verkar involvera unika morfologiska och molekylära mekanismer. Vi visar dessutom att komplexiteten hos de vedartade vävnaderna leder till ett behov av bättre anpassade verktyg för att djupare kunna bedöma PCD och liknande fenomen i veden.
Även med namnet Moreau-Courtois, Charleen L. samt Moreau, Charleen.
Klassen, Shaun Scott. "Nitric oxide-induced cardiomyocyte cell death." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31539.
Повний текст джерелаMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50832.pdf.
Повний текст джерелаMaianski, Nikolai. "Neutrophil cell death: mechanisms and regulation." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/88280.
Повний текст джерелаMartinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21605.
Повний текст джерела8-Iso-PGF2alpha (1--10 nM) induced 20--25% cell death in endothelial cultures after 24 h coincident with similar increase in the number of cells that become permeable to PI. On the contrary, 8-iso-PGE 2 did not affect endothelial cell survival. Approximately 9% of the cells suffered apoptosis. This percentage remained unchanged regardless the treatment. Several observations indicate a role for thromboxane A2 to mediate 8-iso-PGF2alpha-induced death: (1) the levels of thromboxane A2 increased dramatically in endothelial cultures after 8-iso-PGF2alpha-treatment; (2) inhibitors of thromboxane synthase, CGS12970 and U6355A and Ibuprofen, a non-selective inhibitor of cyclooxygenases, reverted the effect of the isoprostane; (3) analogs of thromboxane A2 U46619 and IBOP, reproduce the effect of 8-iso-PGF 2alpha after 24 h. 8-Iso-PGF2alpha also decreased endothelial viability on isolated brain microvessels. These results suggest, that 8-iso-PGF2alpha, might be a direct contributor to ischemia/reperfusion injury.
Spanos, Sophia. "Cell death during preimplantation embryo development." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398228.
Повний текст джерелаŚwidziński, Jodi A. "Programmed cell death in Arabidopsis thaliana." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:6e2580fc-8873-4722-89f7-b206d4be2a5f.
Повний текст джерелаCox, Orla T. "Vascular cell death in diabetic retinopathy." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343079.
Повний текст джерелаSharma, Pundrique Radheyshyam. "Programmed cell death during heart development." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272255.
Повний текст джерелаFitzgerald, Julia. "Monoamine oxidase in neuronal cell death." Thesis, Nottingham Trent University, 2008. http://irep.ntu.ac.uk/id/eprint/51/.
Повний текст джерелаRamos, Paulina Joanna. "Fibronectin Enhances Carfilzomib Mediated Cell Death." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579327.
Повний текст джерелаOrchard, Craig Brailsford. "Relationship between programmed cell death and the cell cycle in the tobacco BY-2 cell line." Thesis, Cardiff University, 2004. http://orca.cf.ac.uk/55931/.
Повний текст джерелаGanz, Michal. "Investigation of growth factors and cytokines that suppress adult stem cell asymmetric cell kinetics." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33874.
Повний текст джерелаIncludes bibliographical references (leaves 40-43).
Adult stem cells are potentially useful in many biomedical applications that can save lives and increase the quality of a patient's life, such as tissue engineering, cell replacement, and gene therapy. However, these applications are limited because of the difficulty in isolating and expanding pure populations of adult stem cells (ASCs). A major barrier to ASC expansion in vitro is their property of asymmetric cell kinetics. Our lab has developed a method, Suppression of Asymmetric Cell Kinetics (SACK), to expand ASCs in vitro by shifting their cell kinetics program from asymmetric to symmetric. We have found that guanine nucleotide precursors can be used to convert the kinetics of adult stem cells from asymmetric to symmetric, which promotes their exponential expansion. Previously, we have used the SACK method to derive hepatic and cholangiocyte stem cell strains from adult rat livers in vitro. These cell strains provide an assay to evaluate whether growth factors and cytokines previously implicated in proliferation of progenitor cells act by converting the kinetics of the stem cells in the population from asymmetric to symmetric, and thus identify new SACK agents. We are evaluating three agents, Wnt, IGF- 1, and Sonic hedgehog (Shh).
(cont.) Wnt has been found to cause self-renewal and proliferation of hematopoietic stem cells (HSCs) in vitro. IGF- 1 also plays a role in hematopoietic progenitor self-renewal in vivo as well as in tissue maturation. Shh has been implicated in the proliferation of primitive neural cells as well as in cellular proliferation during invertebrate development. Thus far, we have found that Wnt peptide shifts the cell kinetics from asymmetric to symmetric and may reduce the generation time, whereas IGF-1 appears only to affect generation time. Studies involving Shh are currently underway. We are also currently investigating whether Wnt acts additively or synergistically with guanine nucleotide precursors to shift cell kinetic symmetry. Discovering new SACK agents will allow us to obtain purer populations of ASCs that can be used to study properties unique to stem cells. Furthermore, the observation that Wnt shifts the kinetics of adult rat hepatic stem cells from asymmetric to symmetric implicates the involvement of similar cell kinetics symmetry mechanisms in the proliferation effect of Wnt on murine and human HSCs.
by Michal Ganz.
S.M.
Edwards, Joanna Marie. "Cell survival and cell death: Role of potassium channels in Alzheimer's disease." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487723.
Повний текст джерелаHoopes, Justin Darrel. "Mechanisms of Induced Cell Death in Bluetongue Virus Challenged Human Cell Lines." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/252.
Повний текст джерелаBerry, David (David A. ). "Glycosaminoglycan regulation of cell function." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/34153.
Повний текст джерелаIncludes bibliographical references (p. 252-285).
Glycosaminoglycans (GAGs) are complex polysaccharides that exist both on the cell surface and free within the extracellular matrix. The intrinsic sequence variety stemming from the large number of building blocks that compose this biopolymer leads to substantial information density as well as to the ability to regulate a wide variety of important biological processes. With the recent and progressive emergence of biochemical and analytical tools to probe GAG structure and function, efforts can be taken to understand the role of GAGs in cell biology and in disease in the various physiological locations where GAGs can exist. As a first step to probe the functions of GAGs, the heparin/heparan sulfate-GAG (HSGAG)-fibroblast growth factor (FGF) system was examined. Understanding the role of HSGAGs in inducing FGF2 dimerization led to the development of a novel engineered protein that was found to be effective at promoting functional recovery in stroke. Subsequently, methods to isolate HSGAGs from the cell surface were optimized and the ability of HSGAGs to support FGF signaling was investigated. Cell surface HSGAGs can define the responsiveness of a given cell to FGF1 and FGF2 through multiple receptor isoforms. Stromal cell derived HSGAGs were also identified as critical regulators of tumor cell growth and metastasis, effecting not only FGF2., but also 1-integrin signaling.
(cont.) Other GAGs, including dermatan sulfates, were characterized as modulators of FGFs and vascular endothelial growth factors. Finally, FGFs and HSGAGs were found to have important roles in maintaining epithelial monolayer integrity, with syndecan-l serving as a critical factor in inflammatory bowel disease. In addition to understanding HSGAGs in their normal physiological settings, techniques to internalize them were developed. Poly(3-amino ester)s were found to condense heparin and enable its endocytosis into cells. Internalized heparin is preferentially taken up by cancer cells, which often have a faster endocytic rate than non-transformed cells, and promotes apoptotic cell death. Internalized heparin can also be used as a tool to probe cell function. In Burkitt's lymphoma, poly(3-amino ester)-heparin conjugates served to identify cell surface HSGAGs as an important modulator of cell growth that can be harnessed to inhibit growth. Finally, studies that sought to broaden the scope of GAG biology were undertaken. Cell surface HSGA(:is were identified as mediators of vascular permeability. Furthermore a novel technique to immobilize GAGs was employed. The interactions between GAG and substrate were via hydrogen bonding. Immobilization of GAGs alters their properties, such that they can affect cells in ways distinct from GAGs free in the ECM.
(cont.) Furthermore, immobilized GAGs can regulate cancer cell adhesion, growth and progression, and may offer a new way to regulate the activity of cancer cells. In addition to directly providing new potential therapeutics and drug targets, these studies represent a foundation to enable additional studies of GAG function. Future work harnessing the techniques presented may open new avenues of research and facilitate the development of novel GAG-based therapeutics.
by David Berry.
Ph.D.
Rosenthal, Adam D. (Adam David) 1978. "Cell patterning technology for controlling the stem cell microenvironment." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39007.
Повний текст джерелаIncludes bibliographical references (leaves 93-101).
Embryonic stem cells serve as powerful models for the study of development and disease and hold enormous potential for future therapeutics. Yet, over two decades after mouse embryonic stem cells (mESCs) were first isolated, there is still little known about the role of cell-cell signaling in self-renewal. Since traditional cell-culture techniques do not provide significant control of the stem cell microenvironment, the goal of this thesis was to develop a cell patterning technology that allows us to precisely control stem cell signaling and monitor cell proliferation over time. In the first aim of this thesis, we describe the development of our first cell patterning technology using dielectrophoresis (DEP). DEP uses nonuniform electric fields to trap cells on or between electrodes. We first used beads as model particles to validate the strength of our DEP square trap, and then demonstrated efficient cell patterning with multiple cell types. In the second aim of this thesis, we describe the development of a novel cell patterning technology that we created, called the Bio Flip Chip (BFC).
(cont.) The BFC is a microfabricated polymer chip, containing thousands of microwells, that enables cell patterning with single-cell resolution anywhere on a substrate and onto any substrate. In the last aim of this thesis, we used our BFC technology to control the stem cell microenvironment, allowing us to incrementally and independently modulate cell-cell contact. We present the first quantitative evidence that cell-cell contact depresses mESC colony formation and show that E-cadherin signaling is responsible for this negative regulatory pathway.
by Adam Rosenthal.
Ph.D.
Dyche, G. H. "IAA production during cell division and xylogenesis." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384461.
Повний текст джерелаPatient, Michaela Eileen. "Rcd, a ColE1-encoded cell division inhibitor." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309210.
Повний текст джерелаHung, Yuen-mang Venus, and 洪婉萌. "Meaningful learning of cell division and genetics." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/209665.
Повний текст джерелаpublished_or_final_version
Education
Master
Master of Education
Fowler, M. R. "Gene expression during sugar beet cell division." Thesis, De Montfort University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264308.
Повний текст джерелаTrambaiolo, Daniel Marco. "Crystallographic studies of bacterial cell division proteins." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611977.
Повний текст джерела