Rozprawy doktorskie na temat „Cell Metabolism”
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Pat, Sze Wa. "Cell metabolism in cell death and cell growth". HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.
Pełny tekst źródłaIafelice, Bruno <1979>. "Miniaturized sensors for cell metabolism". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/397/1/Tesi_encripted.pdf.
Pełny tekst źródłaIafelice, Bruno <1979>. "Miniaturized sensors for cell metabolism". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/397/.
Pełny tekst źródłaChowdhury, Azazul Islam. "Role of Cell-cell Interactions and Palmitate on β-cells Function". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230841.
Pełny tekst źródłaBoard, Mary. "A study of energy metabolism in neoplastic cells". Thesis, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:d3e13e31-3fe8-4cd8-ad71-50d4e7df4d27.
Pełny tekst źródłaSidiq, Karzan Rafiq. "Cell wall metabolism in Bacillus subtilis". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3243.
Pełny tekst źródłaTilney-Bassett, Amanda L. "Phospholipid metabolism in T-cell activation". Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239331.
Pełny tekst źródłaTueller, Josephine Anna. "Investigation of Therapeutic Immune Cell Metabolism". BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8704.
Pełny tekst źródłaThomas, Geraint Mark Howard. "Lithium and phosphoinositide metabolism". Thesis, University of Wolverhampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238120.
Pełny tekst źródłaHooper, Nigel Mark. "Metabolism of neuropeptides by cell-surface peptidases". Thesis, University of Leeds, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235486.
Pełny tekst źródłaAlakpa, Enateri V. "Cell metabolism in response to biomaterial mechanics". Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/4970/.
Pełny tekst źródłaGupta, Sneha Veeraraghavan. "Targeting Protein Metabolism in B-cell Malignancies". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1343169973.
Pełny tekst źródłaLi, Zhaoqi Ph D. Massachusetts Institute of Technology. "Bioenergetics and metabolism of eukaryotic cell proliferation". Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/130658.
Pełny tekst źródłaCataloged from the official PDF of thesis. "February 2021." Vita. Page 179 blank.
Includes bibliographical references.
Cellular growth and proliferation necessitates the transformation of cell-external nutrients into biomass. Strategies of biomass accumulation across the kingdoms of life are diverse and range from carbon fixation by autotrophic organisms to direct biomass incorporation of consumed nutrients by heterotrophic organisms. The goal of this dissertation is to better understand the divergent and convergent modes of metabolism that support biomass accumulation and proliferation in eukaryotic cells. We first determined that the underlying mechanism behind why rapidly proliferating cells preferentially ferment the terminal glycolytic product pyruvate is due to an intrinsic deficiency of respiration to regenerate electron acceptors. We tested this model across an assorted array of proliferating cells and organisms ranging from human cancer cells to the baker's yeast Saccharomyces cerevesiae. We next determined that a major metabolic pathway of avid electron acceptor consumption in the context of biomass accumulation is the synthesis of lipids. Insights from this work has led to the realization that net-reductive pathways such as lipid synthesis may be rate-limited by oxidative reactions. Lastly, we established the green algae Chlorella vulgaris as a model system to study the comparative metabolism of photoautotrophic and heterotrophic growth. We determined that heterotrophic growth of plant cells is associated with aerobic glycolysis in a mechanism that may be suppressed by light. Collectively, these studies contribute to a more holistic understanding of the bioenergetics and metabolic pathways employed by eukaryotic cells to accumulate biomass and lay the foundation for future studies to understand proliferative metabolism.
by Zhaoqi Li.
Ph. D. in Biochemistry
Ph.D.inBiochemistry Massachusetts Institute of Technology, Department of Biology
Nunan, Kylie. "Cell wall metabolism in developing grape berries /". Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09APSP/09pspn972.pdf.
Pełny tekst źródłaTejedor, Vaquero Sonia 1988. "Influence of metabolism in the regulation of T cell differentiation". Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/664638.
Pełny tekst źródłaLa glucosa és un nutrient essencial per les cèl·lules T. Malgrat que l’activació T es veu disminuïda per la manca de glucosa, s’ha vist que respostes T efectores tenen lloc in vivo en entorns amb nivells baixos de glucosa, com són els tumors. Això planteja la incògnita de saber com aquestes cèl·lules poden mantenir les seves funcions en ambients pobres de nutrients. En aquest treball hem analitzat la capacitat de les cèl·lules T efectores (Th0) de ser activades en condicions pro-inflamatòries i nivells baixos de glucosa (0.3 mM). Hem vist que les cèl·lules T efectores secundàries poden induir citocines característiques de respostes Th1 i Th17 com la IL-17A i l’IFNγ en condicions de nivells baixos de glucosa, però perden la capacitat d’expressar la IL-22. Aquestes cèl·lules s’adapten a un entorn baix de glucosa reduint-ne el consum i reduint l’expressió de gens de la glicòlisi, malgrat tot, la glucosa segueix sent la seva principal font d’energia (ATP). A més a més, hem observat que nivells limitats de glucosa provoquen una lleu però progressiva deficiència en l’activitat d’mTORC1, necessària per la producció de la IL-22 i que explicaria en part la disminució dels nivells d’aquesta citocina. Els nostres resultats també mostren que les cèl·lules T efectores secundàries que han experimentat un estrès de glucosa adquireixen un fenotip de memòria que fa que responguin de manera alterada (producció exagerada de IL-22) a un segon estímul en presència de nivells normals de glucosa. Finalment, hem observat que les cèl·lules T CD4 efectores activades in vivo expressen diferencialment gens sensibles a glucosa quan són re-estimulades ex vivo. Això suggereix que el context d’activació d’una cèl·lula T és important per determinar la resposta d’aquestes cèl·lules a posteriors estimulacions en situació de baixa glucosa. En resum, els nostres resultats mostren que els limfòcits T son capaços de mantenir un ventall de funcions efectores en situacions de restricció de nutrients, però que el haver passat per una etapa d’estrès de nutrients pot condicionar els seus perfils d’expressió gènica en respostes efectores futures.
Xue, Yue 1978. "Iron metabolism in mammalian cells". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79216.
Pełny tekst źródłaIron Regulatory Proteins (IRPs), which serve as main posttranscriptional regulators of cellular iron homeostasis, are the other interest of research. Iron regulatory proteins reversibly interact with iron regulatory elements (IREs) within ferritin and transferrin receptor (TfR) mRNAs. The binding ability of IRPs is under tight control so that they respond to the changes in the intracellular iron requirements in a coordinate manner by differentially regulating ferritin mRNA translational efficiency and TfR mRNA stability. Besides intracellular iron levels, some other stimuli, such as oxidative stress, are capable of regulating this RNA-protein interactions.
Liu, Laura Xiaofei-Rose. "Maternal Cardiac Metabolism during Pregnancy". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17465316.
Pełny tekst źródłaMedical Sciences
Dolatshahi, Marjan. "Conformational changes of polyomavirus during cell entry". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111604.
Pełny tekst źródłaBreznan, Dalibor. "High-density lipoprotein metabolism in the kidney". Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6120.
Pełny tekst źródłaMashhedi, Haider. "Implicating insulin in neoplastic growth and metabolism". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104681.
Pełny tekst źródłaCompte tenu de l'accumulation de preuves liant l'obésité à un nombre accru de cancers, il y a un grand intérêt à définir les mécanismes par lesquels l'obésité influe sur la croissance néoplasique. Des niveaux d'insuline élevés sont couramment associés à l'obésité ou au «syndrome métabolique», ce qui fait que le récepteur de l'insuline est considéré comme une cible moléculaire potentiellement importante pour le traitement de certains cancers. Pour étudier les effets de l'atténuation de la signalisation de l'insuline sur la croissance du modèle expérimental du cancer du sein chez la souris, la lignée cellulaire insulino-sensible 4T1 in vivo, nous avons comparé les effets d'une déficience à l'insuline induite par l'alloxan à celle de BMS-536924, un inhibiteur des kinases tyrosine des récepteurs de l'insuline et d'IGF-I. Les deux interventions ont montré une activité anti-néoplasique, mais seulement l'alloxan a présenté une toxicité métabolique. L'inhibition des récepteurs d'insuline n'a occasionné qu'une faible hyperglycémie et le traitement avec BMS-536924 a été bien toléré. Nous avons attribué ce phénomène à des facteurs pharmacocinétiques en mesurant l'accumulation de drogue dans les tissus et pour déterminer si le BMS-536924 abolit l'absorption insulino-dépendante du glucose, nous avons mesuré la quantité de glucose utilisé dans le muscle. Nos données indiquent que la captation insulino-dépendante du glucose par le muscle est restée intacte. Ainsi, la distribution tissu-spécifique du BMS-536924 peut être responsable de l'activité anti-néoplasique sans toxicité métabolique grave, ce qui indique que le ciblage pharmacologique du récepteur de l'insuline dans la maladie néoplasique peut être efficace.Les études épidémiologiques ont montré que les patients diabétiques de type II prenant le médicament metformine (un biguanide) ont un risque réduit de développer un cancer ou d'un taux de mortalité due au cancer plus faible par rapport aux patients diabétiques de type II suivant d'autres thérapies. Nous avons déjà montré que la metformine agit comme un inhibiteur de la croissance des cellules tumorales in vitro en phosphorylant l'AMPK d'une manière dépendante de la dose. Outre l'activation de l'AMPK, qui est observée dans les cellules tumorales in vitro et in vivo, la metformine provoque aussi une diminution des taux d'insuline. Ceci est un effet secondaire de la réduction du taux de glycémie dans un contexte de diabète de type II. La tomographie par émission de positons (TEP ou PET) est une technique d'imagerie qui mesure le taux d'utilisation du glucose par les cellules cancéreuses à l'aide de l'analogue du glucose radiomarqué 18F-2-Fluoro-2-Désoxy-D-Glucose (FDG). Nous étions intéressés par les effets de la metformine sur la captation du glucose par les tumeurs d'adénocarcinome de côlon, MC38, allogreffées chez des souris qui ont été nourris avec une diète à haute teneur énergétique (induisant un phénotype diabétique de type II), ou un régime contrôle. Nos résultats montrent que la metformine abolie l'augmentation des niveaux sériques d'insuline, l'activation du récepteur d'insuline dans les tumeurs ainsi que l'absorption du FDG par les tumeur chez les souris ayant un régime riche en énergie et que la metformine n'a aucun effet sur ces mesures chez les souris ayant une diète contrôle. Ceci suggère que pour un sous-ensemble de néoplasmes, le régime alimentaire et le taux d'insuline influencent l'absorption du glucose par les cellules tumorales ce qui pourrait avoir une pertinence clinique dans les prochaines études clinique visant l'évaluation de l'activité anti-néoplasique de la metformine.
Kensley, Joy A. "Glycogen metabolism in Corynebacterium glutamicum ATCC 13032". Doctoral thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/4279.
Pełny tekst źródłaCorynebacterium glutamicum is a Gram-positive facultative aerobe particularly known for its industrial application in the synthesis of amino acids, such as L-glutamate and Llysine. The central metabolic pathways of this organism has been an area of much research by many groups. Linked to glycolysis is the synthesis of glycogen, previously considered a storage molecule of excess glucose. No information concerning the role of glycogen or its metabolism in C. glutamicum was known, and the aim of this work was to elucidate glycogen metabolism in this industrially important organism.
Schulz, Anton A. "Nitrogen metabolism in Corynebacterium glutamicum ATCC 13032". Doctoral thesis, University of Cape Town, 2002. http://hdl.handle.net/11427/4329.
Pełny tekst źródłaCorynebacterium glutamicum is extensively used for the commercial production of a host of amino acids including lysine, glutamate, and threonine. Consequently, much research has been directed at analyzing nitrogen metabolism in this bacterium. In particular, our research focused on investigating the regulation of nitrogen assimilation. Initially, we searched for homologs of the Streptomyces glnR, glnII, and glnE genes in C. glutamicum. These studies, however, were met with limited success, and we therefore decided to use promoter probe vectors in order to identify nitrogen-responsive promoters.
Johnson, Jenifer L. "Development of redox microphysiometry to assay cell signaling and metabolism /". Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8498.
Pełny tekst źródłaJani, Klodiana. "The role of integrin-dependent cell matrix adhesion in muscle development /". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115688.
Pełny tekst źródłaWe demonstrate a novel role for the PDZ/LIM domain protein Zasp as a core component of Integrin adhesions. Specifically, Zasp colocalizes with Integrins at focal adhesion in cultured cells and myotendinous junctions in Drosophila embryos. In both cases elimination of Zasp modifies Integrin function causing consequently defects in cell spreading and muscle attachment. Zasp supports Integrin adhesion to the extracellular matrix that is required to withstand tensile forces exerted during cell spreading and muscle contraction. Furthermore, we found that the distribution of Zasp in muscle Z-lines is essential to orchestrate the cross-linking of alpha-Actinin and Actin filaments. Disruption of Zasp leads to loss of muscle cytoarchitecture, pointing to a larger role for Zasp in sarcomere assembly. Finally, we demonstrate that Zasp, in addition to alpha-Actinin, physically interacts with the Integrin- and Actin-bound cytoskeletal protein Talin.
Collectively, our results point to a dual role for Zasp as a structural scaffold. First it regulates Integrin adhesion to the extracellular matrix by interacting with the head domain of Talin at the myotendinous junctions. Second, Zasp controls sarcomere assembly by tethering the presarcomeric alpha-Actinin component to the tail domain of Talin. Zasp finding as a crucial adhesion component provides further insights on the mechanism underlying Integrin-mediated adhesion.
To, Wing Shu. "Effect of cellular redox and energy states on benzo[a]pyrene induced modes of death in the hepa and the HepG2 cell lines". HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1173.
Pełny tekst źródłaSurmann, Eva-Maria. "Connections between tumour suppression and cellular metabolism". Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709136.
Pełny tekst źródłaPinent, Armengol Montserrat. "Adipose cell metabolism modulation by red wine procyanidins". Doctoral thesis, Universitat Rovira i Virgili, 2005. http://hdl.handle.net/10803/8650.
Pełny tekst źródłaagainst pathologies such as cardiovascular heart disease and related illnesses. Although
adipose tissue has a central role in some of these pathologies, including obesity and diabetes,
there is a lack of information about the effects of procyanidins on this tissue. This thesis
addresses this question. The effects of a grape seed procyanidin extract (GSPE) on the lipid
and glucose metabolism of adipocytes were evaluated by taking the 3T3-L1 cell line as a
model of study. Results show that the GSPE has insulinomimetic effects, stimulating glucose
uptake, glycogen synthesis and trigliceride synthesis. To achieve this, the GSPE shares some
of the mechanisms and intracellular mediators of the insulin-signalling pathways (such as
GLUT-4 translocation, PI3K and p38 MAPK) but it must also use other, complementary,
mechanisms. These results suggest that procyanidins have beneficial effects on diabetes
and/or insulin resistance. This is partially proven by in vivo studies that show that GSPE has
antihyperglycemic properties on streptozotozin-induced diabetic rats. Also analyzed in this
thesis are the molecular mechanisms used by GSPE to explain the already described lipolytic
effects. Protein kinase A and PPARã are shown to be involved in these effects. Some of
these results opened up another line of study into the effects of GSPE on the differentiation
process of the 3T3-L1. These studies showed that procyanidins alter the differentiation of
preadipocytes when added at the induction of differentiation. Since an increase in the
number of adipocytes has a negative effect on obesity, this is a promising characteristic of
GSPE that should be taken into account when its possible antiobesity properties are studied.
Als flavonoides, i més concretament a les procianidines del vi negre, se'ls han atribuït moltes
propietats beneficioses contra diverses patologies, com les malalties cardiovasculars i altres
patologies relacionades. Tot i que el teixit adipós juga un paper important en algunes
d'aquestes patologies, com la obesitat i la diabetis, la informació referent l'acció de les
procianidines en aquest teixit és escassa. Aquesta tesis estudia els efectes de les procianidines
derivades de pinyol de raïm (GSPE) en l'adipòcit, i per a dur-ho a terme es pren com a
model d'estudi la línia cel.lular 3T3-L1. Per una banda es descriuen els efectes del GSPE en
el metabolisme de lípids i glúcids de la cèl.lula adiposa. El GSPE fa un paper
insulinomimètic: estimula la captació de glucosa, la síntesi de glicògen i la síntesi de triacil
glicerols. L'anàlisi dels mecanismes moleculars per exercir aquests efectes mostra que GSPE
en part comparteix mecanismes i vies de senyalització propis de la insulina (translocació de
GLUT-4, PI3K, p38 MAPK); tanmateix, s'observa que GSPE ha d'usar també altres
mecanismes complementaris. Aquests resultats suggereixen que GSPE pot tenir efectes
positius en situacions de diabetis i/o resistència a insulina, donat que a més a més, els estudis
in vivo mostren que GSPE és antihiperglicèmic en condicions de diabetis induïda per
estreptozotocina. En aquesta tesis també s'analitzen els mecanismes moleculars que
explicarien els efectes lipolítics de les procianidines descrits en estudis previs, i s'ha trobat
que la proteina kinasa A i PPARã hi estan involucrats. Part d'aquests resultats han obert una
altra via d'estudi sobre els efectes de la GSPE en el procés de diferenciació de la cèl.lula
adiposa on s'ha observat que el tractament amb procianidines a l'inici de la diferenciació
dificulta aquesta transformació. Donat que l'augment del nombre d'adipòcits afecta
negativament la obesitat, aquest efecte de les procianidines és una característica
prometedora que caldrà tenir en compte en l'estudi del seu possible paper antiobesitat.
Saridogan, Ertan. "Cell biology and metabolism of human Fallopian tube". Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286201.
Pełny tekst źródłaBibby, Susan R. S. "Cell metabolism and viability in the intervertebral disc". Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249331.
Pełny tekst źródłaSimon, Charles. "Novel resveratrol analogues : synthesis, metabolism and cell proliferation". Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9289.
Pełny tekst źródłaHung, Yin Pun. "Single Cell Imaging of Metabolism with Fluorescent Biosensors". Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10147.
Pełny tekst źródłaSinghal, Atul. "Growth and metabolism in homozygous sickle cell disease". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288009.
Pełny tekst źródłaHudson, Michael John. "Monoterpene metabolism of Mentha and its cell cultures". Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37729.
Pełny tekst źródłaRoohi, Aysha. "Toxoplasma gondii infection and the host cell metabolism". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648369.
Pełny tekst źródłaGreen, Martha Alexandra. "Apoplastic ascorbate metabolism in rose cell suspension cultures". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/14944.
Pełny tekst źródłaChaneton, Barbara Julieta. "Targeting cancer cell metabolism as a therapeutic strategy". Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5762/.
Pełny tekst źródłaWei, Hsi-Ju. "TARGETING DENDRITIC CELL METABOLISM TO INDUCE IMMUNE TOLERANCE". Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1538497998943838.
Pełny tekst źródłaZancanaro, Krauss Maria Eduarda. "CD4+ T cell metabolism during Trichuris muris infection". Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/cd4-t-cell-metabolism-during-trichuris-muris-infection(24eb0cc7-db70-46ea-ba49-e4fe3d5a5d03).html.
Pełny tekst źródłaCASATTA, NADIA. "Exploring the metabolism beyond cell aging in yeast". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41494.
Pełny tekst źródłaBHARAT, ROHIT. "Targeting cancer cell metabolism: Gateway towards personalized medicine". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241161.
Pełny tekst źródłaIn the recent decade, one of the important keynote message derived through the summation of our global efforts against cancer is the need to better understand cancer cell metabolism for the development of better and efficacious personalized therapy. Cancer cells undertake a multifaceted rewiring of metabolic pathways in order to support their proliferative and invasive nature, which requires a systems level investigation to fully comprehend the scale of metabolic deregulation. In this study, we systematically investigated the metabolic differences using untargeted metabolomics and 13C flux omics approach in oncogenic K-Ras driven tumours. We tested the effects of drug inhibitors targeting glucose and glutamine metabolism to unravel the alternative metabolic pathways required for cancer cell survival. We further expanded our research towards understanding the role of cellular metabolism in driving resistance to endocrine therapeutic drugs in ERα positive breast cancer. We identified specific metabolic mechanisms of utilization of glutamine in resistant cells while also providing further basis for the use of metformin as an adjuvant in the treatment of endocrine therapyresistant cancers. Finally, we contributed to current understanding about cancer cell metabolism by exploring the role of glutamine beyond its role as a carbon and nitrogen source in driving growth and proliferation of cancer cells. Upon substitution of glutamine with appropriateiv nitrogen and carbon sources, cancer cells exhibited reverse Warburg phenotype. The findings from this thesis open up new avenues of research through the identification of new putative targets and bring us one step closer towards designing much better and efficacious therapeutic strategy for the treatment of cancer patients.
Sujareerat, Charin. "Development of L1210 mutants in NAD metabolism". Thesis, University of Bath, 1989. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235333.
Pełny tekst źródłaKrzywinska, Ewelina. "Study of tumor cell metabolism and its relationship with NK cell-mediated immunotherapy". Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON1T012/document.
Pełny tekst źródłaTumor formation and development are caused by a range of defects that occur inside the cancer cell and in the external cellular microenvironment. These abnormalities allow developing tumors to establish their own strategies of growth, proliferation, differentiation and metabolism. All these adaptations, as well as the creation of a unique microenvironment, promote tumor growth and suppress the anti-cancer immune response. Tumor cell metabolism and immune evasion are sensitive points of cancer development that can be targeted in clinic. Recent studies suggest that these two phenomena are related and that cancer cell metabolism may propel tumor immune escape. Tumor cell metabolism tends to avoid mitochondrial activity and oxidative phosphorylation (OXPHOS), and largely relies on glycolysis to produce energy (Warburg effect). My thesis work is divided into two parts. The first one proposes an innovative therapeutic strategy, which is the use of different combinatorial therapy depending on the p53 status for the treatment of hematological cancers. This is based on the induction of metabolic changes by dichloroacetate (DCA), combined with conventional chemotherapy (doxorubicin, vincristine) to reactivate wild type p53 functions. Mutant p53 tumors are resistant to this combination approach. However, we found that DCA synergized with the Hsp90 inhibitor 17-AAG to specifically eliminate these cells. Therefore, a clearer understanding of the signals and mechanisms by which DCA sensitize cancer cells to chemotherapy was needed to understand its mode of action. We uncovered it in our work. In addition, identification of this mechanism will help to elucidate metabolic pathways involved in cancer cell survival.The second part of my thesis is focused on the study of NK cell biology. NK cell is an innate immune system lymphocyte lineage with natural cytotoxicity against targets, i.e. tumor cells. Its optimal use in the clinic requires in vitro expansion and activation. Cytokines and the encounter with target cells activate NK cells, induce their proliferation, and cause clearly different mRNA/miRNA expression profile. Detailed analysis of the leucocyte-specific phosphatase CD45 isoforms allowed us to characterize new human anti-tumor NK cell populations. The identification of the different NK cell populations is important for understanding their physiology and for improving their therapeutic use in the clinic. It can also give valuable information about the host physiological status. Indeed, the increase of CD45RAdim and CD45RO+ cells in the mature NK cell compartment clearly identifies patients with hematological malignancies. We thus hypothesize that their detection could be used as a diagnostic tool, and also to assess the efficacy of antitumor treatments, because these specific NK cell populations should decrease upon removal of the targeted tumor cells. Our future goal is to use a novel combinatorial therapy in hematological cancers that will combine metabolic drugs and NK cell-based therapy. Based on our preliminary data, we propose that the treatment of cancer cells with metabolic drugs could increase their sensitivity and recognition by activated NK cells
Escoté, Miró Xavier. "Control of cell cycle progression by the last MAPK Hog1". Doctoral thesis, Universitat Pompeu Fabra, 2005. http://hdl.handle.net/10803/7186.
Pełny tekst źródłaDimasi, Don. "A mechanistic analysis of mammalian cell metabolism in continuous culture /". Thesis, Connect to Dissertations & Theses @ Tufts University, 1992.
Znajdź pełny tekst źródłaSubmitted to the Dept. of Chemical Engineering. Adviser: Randall W. Swartz. Includes bibliographical references (leaves 243-247). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
Lähdesmäki, Ilkka Johannes. "Flow injection methods for drug-receptor interaction studies, based on probing cell metabolism /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8590.
Pełny tekst źródłaNilsson, Harriet. "The role of nitric oxide in cytoskeleton-mediated organelle transport and cell adhesion /". Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med660s.pdf.
Pełny tekst źródłaTheret, Marine. "Cell and non-cell autonomous regulations of metabolism on muscle stem cell fate and skeletal muscle homeostasis". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB120/document.
Pełny tekst źródłaDuring skeletal muscle regeneration, muscle stem cells activate and recapitulate the myogenic program to repair the damaged myofibers. A subset of these cells does not enter into the myogenesis program but self-renews to return into quiescence for further needs. Control of muscle stem cell fate choice is crucial to maintain homeostasis but molecular and cellular mechanisms controlling this step are poorly understood. A difficulty of understanding muscle stem cell self-renewal is that skeletal muscle regeneration is a coordinated and non-synchronized process. Various and dissociated molecular and cellular mechanisms regulate muscle stem cell fate. Indeed, skeletal muscle regeneration requires the interaction between myogenic cells and other cell types, among which the macrophages. Macrophages infiltrate the muscle and adopt distinct and sequential phenotypes. They act on the sequential phases of muscle regeneration and resolving the inflammation by skewing their inflammatory profile to an anti-inflammatory state. Some in vitro studies suggested a role for the metabolism and the AMP-activated protein Kinase (AMPK), the master metabolic regulator of cells, in both inflammation and stem cell fate. Thus, I investigated the role of metabolism on muscle stem cell fate within the muscle stem cells (cell autonomous regulations) and through the action of macrophages (non-cell autonomous regulations) during skeletal muscle regeneration. To analyze muscle stem cell fate, I used in vitro (macrophages and muscle stem cell primary cultures), ex vivo (isolated myofibers) and in vivo (using specific mice model deleted specifically for AMPK1 in the myeloid lineage, in muscle stem cells or in myofibers) experiments. First, I highlighted that macrophagic AMPK1is required for the resolution of inflammation during skeletal muscle regeneration and for the trophic functions of macrophages on muscle stem cell fate. Moreover, CAMKK-AMPK1 activation regulates phagocytosis, which is the main cellular mechanism inducing macrophage skewing. This work was published in 2013 in Cell Metabolism. Second, I demonstrated that depletion of myogenic AMPK1 tailors muscle stem cell metabolism in a LKB1 independent manner, orients their fate to the self-renewal by promoting metabolic switch from an oxidative to a glycolytic metabolism pathway, through the over activation of a new molecular target, which is a key enzyme for glycolysis: the Lactate Dehydrogenase. To conclude, during my thesis, I established two new crucial roles of AMPK1 in muscle stem cell fate choice, linking for the first time metabolism, inflammation and fate choice
Westermark, Pål. "Models of the metabolism of the pancreatic beta-cell". Doctoral thesis, KTH, Numerical Analysis and Computer Science, NADA, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-408.
Pełny tekst źródłaThe pancreatic β-cell secretes insulin in response to a raised blood glucose level. Deficiencies in this control system are an important part of the etiology of diabetes. The biochemical basis of glucose-stimulated insulin secretion is incompletely understood, and a more complete understanding is an important component in the quest for better therapies against diabetes.
In this thesis, mathematical modeling has been employed in order to increase our understanding of the biochemical principles that underlie glucosestimulated insulin secretion of the pancreatic β-cell. The modeling efforts include the glycolysis in theβ-cell with particular emphasis on glycolytic oscillations. The latter have earlier been hypothesized to be the cause of normal pulsatile insulin secretion. This model puts this hypothesis into quantitative form and predicts that the enzymes glucokinase and aldolase play important roles in setting the glucose concentration threshold governing oscillations. Also presented is a model of the mitochondrial metabolism in the β-cell, and of the mitochondrial shuttles that connect the mitochondrial metabolism to the glycolysis. This model gives sound explanations to what was earlier thought to be paradoxical behavior of the mitochondrial shuttles during certain conditions. Moreover, it predicts a strong signal from glucose towards cytosolic NADPH formation, a putative stimulant of insulin secretion. The model also identifies problems with earlier interpretations of experimental results regarding the β- cell mitochondrial metabolism. As an aside, an earlier proposed conceptual model of the generation of oscillations in the TCA cycle is critically analyzed.
Further, metabolic control analysis has been employed in order to obtain mathematical expressions that describe the control by pyruvate dehydrogenase and fatty acid oxidation over different aspects of the mitochondrial metabolism and the mitochondrial shuttles. The theories developed explain recently observed behavior of these systems and provide readily testable predictions.
The methodological aspects of the work presented in the thesis include the development of a new generic enzyme rate equation, the generalized reversible Hill equation, as well as a reversible version of the classical general modifier mechanism of enzyme action.
Pryjma, Mark Christopher. "Campylobacter jejuni metabolism in survival and host cell interactions". Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/48597.
Pełny tekst źródłaScience, Faculty of
Microbiology and Immunology, Department of
Graduate
Papas, Klearchos Kyriacos. "Bioenergetics, metabolism, and secretion of immunoisolated endocrine cell preparations". Thesis, Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/11001.
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