Global ETD Search

1	L'encéphalite à auto-anticorps anti-NMDAR, un modèle de synaptopathie / NMDAR Encephalitis, a model of synaptopathy Chefdeville, Aude 11 December 2017 (has links) Que se passe-t-il quand le système immunitaire attaque le cerveau ? Dans l'encéphalite à autoanticorps dirigés contre les récepteurs NMDA, le système immunitaire des patients dysfonctionne : au lieu de produire des anticorps pour combattre des organismes pathogènes, le système immunitaire produit des anticorps qui attaquent une protéine spécifique dans le cerveau des patients, les récepteurs NMDA. Ces récepteur sont indispensables à la mémoire et sont impliqués dans diverses maladies (schizophrénie, maladie d'Alzheimer). Les patients atteints d'encéphalite à autoanticorps dirigés contre les récepteurs NMDA souffrent de troubles neuropsychiatriques sévères (hallucinations, paranoïa, mouvements anormaux, épilepsie, amnésie, etc.) et la gravité de leur état de santé nécessite une prise en charge en réanimation. Malgré cette sévérité, 8 patients sur 10 récupèrent avec un traitement adapté. Les patients souffrant de cette maladie sont majoritairement des jeunes femmes porteuses d'une tumeur des ovaires. Le premier objectif de ma thèse est de comprendre le rôle de cette tumeur dans le dysfonctionnement du système immunitaire de ces patientes. Mon second objectif est de comprendre comment les autoanticorps attaquant les récepteurs NMDA vont perturber le fonctionnement du cerveau. Apporter des éléments de réponse à ces questions permettra à terme d'améliorer la prise en charge des patients / Anti-NMDA receptor (NMDAR) encephalitis is a rare but severe neuropsychiatric disorder initially described by J. Dalmau and colleagues in 2007. Anti-NMDAR encephalitis is defined by a clinical picture of encephalitis associated with the presence of IgG directed against the GluN1 subunit of NMDAR (NMDAR-Abs) in the cerebrospinal fluid (CSF) of patients. This disorder predominantly affects young women. Clinical presentation usually includes psychiatric symptoms and/or neurological symptoms often accompanied by decreased responsiveness and autonomic instabilities during the course of the disease . Despite the severity of the disease, 81% of patients recover fully or with mild sequels . 38% of patients had an underlying neoplasm, 94% of which were ovarian teratomas , indicating a role for this tumor in the immunopathogenesis of the disease. Studies in vitro and on animal models have demonstrated the pathogenicity of NMDAR-Abs but more studies are required to decipher the pathological role of anti-NMDAR antibodies. Two main research focuses have emerged in our group: understanding the events leading to the immune dysregulation in the ovary teratoma and identifying the pathological element(s) and how they act at the molecular and cellular levels to cause the broad neurological spectrum of symptoms observed in patients. My PhD was especially focused on 1) understanding the involvement of the underlying ovary teratoma in the triggering of the immune response during anti-NMDAR encephalitis and 2) studying the impact of prolonged exposure of the neuronal network to patients’ NMDAR-Abs and the potential involvement of microglial cells in the physiopathology of the disease Encéphalite Autoanticorps NMDAR Tératome Encephalitis Autoantibodies NMDAR Teratoma 612.8
2	Modélisation de l'épithélium bronchique humain par la technologie des cellules souches pluripotentes induites (iPS) / Modelling human bronchial epithelium by induced pluripotent stem cell (iPS) technology. Sansac, Caroline 18 October 2016 (has links) Les cellules souches pluripotentes (CSP) incluent les cellules souches embryonnaires (ES) et les celles souches pluripotentes induites (iPS). Elles sont définies par deux propriétés fondamentales : l’auto-renouvellement et la capacité à se différencier dans tous les types cellulaires. Les ES sont dérivées de la masse cellulaire de l’embryon. Elles soulèvent l’intérêt de la communauté scientifique du fait de leur capacité à générer tous les tissus. Il s’agit d’un outil biotechnologique majeur dont les applications thérapeutiques et pharmacologiques comporteront notamment la médecine régénératrice, la modélisation in vitro de maladies humaines et le criblage de candidat-médicaments. Cependant l’utilisation d’embryons humains pour générer les ES soulève des problèmes éthiques. Les iPS contournent ces difficultés car elles sont dérivées de cellules somatiques différenciées. En effet, S. Yamanaka, qui a reçu le prix Nobel en 2012, a découvert en 2006 une technique simple de reprogrammation cellulaire. L’expression transitoire de quatre gènes (OCT4, SOX2, c-MYC and KLF4) est suffisante pour reprogrammer des fibroblastes murins en iPS. Ces cellules iPS ont la même morphologie et les mêmes propriétés que les cellules ES. L’année suivante, S. Yamanaka a appliqué avec succès son cocktail à des fibroblastes humains pour produire des iPS humaines (hiPS). Les hiPS peuvent également dépasser les problèmes immunologiques soulevés par l’utilisation d’ES dans la thérapie cellulaire, par le simple fait que les hiPS pourront être dérivées du patient à traiter. De plus, parce qu’il est possible de choisir les cellules du donneur à reprogrammer selon son génotype, il est plus facile de modéliser des maladies génétiques à partir d’hiPS que d’ES. Enfin, d’un point de vue pharmaceutique, les hiPS peuvent fournir une plateforme quasi-infinie pour le criblage de molécules afin de traiter diverses pathologies. Le but de mon projet de recherche est l’utilisation de la technologie hiPS afin de modéliser le développement de l’épithélium bronchique. Premièrement, in vivo, des tératomes ont été générés après injection d’hiPS dans des souris immunodéficientes. Les tératomes démontrent la capacité de nos hiPS à se différencier en épithélium bronchique. Secondairement, in vitro, reproduire le développement embryonnaire et fœtal permet d’offrir une méthode simple pour modéliser l’épithélium bronchique dans un puits. Cette technologie ouvre la voie vers de nombreuses recherches, du criblage de molécules à la production de cellules souches pour réparer l’épithélium bronchique, et in fine à la promotion de nouveaux traitements pharmacologiques ou de thérapie innovante pour les maladies respiratoires. / Pluripotent stem cells (PSC) include embryonic stem cells (ES) and induced pluripotent stem cells (iPS). They are defined by two fundamental properties: self-renewal and the capacity to differentiate into all cell types. ES cells are derived from the inner cell mass of embryos. They arouse the interest of the scientific community in particular for their ability to generate all tissues. They provide major therapeutic and pharmacological applications, including regenerative medicine, in vitro modelling of human diseases and molecular screening. However, the use of human blastocysts to generate ES cells raises many ethical problems. iPS circumvent these ethical issues as they can be derived from differentiated somatic tissues. Indeed, S. Yamanaka, Nobel Prize in 2012, discovered in 2006 a simple technique of cellular reprogramming. The transient expression of four genes (OCT4, SOX2, c-MYC and KLF4) is sufficient to reprogram mouse fibroblasts into iPS. These iPS cells have the same morphology and the same properties than ES cells. The following year, S. Yamanaka applied successfully his cocktail to human fibroblasts to produce human iPS (hiPS). hiPS may also overcome immunological problems raised by the use of ES cell for cellular therapy, as hiPS can be derived from the patient to be treated. In addition, it is easier to model genetic diseases from hiPS than ES, because it is possible to choose the donor cells to reprogram according to its genotype. Finally, from a pharmacological point of view, hiPS can provide a broad platform of molecular screening to treat various diseases. The aim of my research project is to use the hiPS technology to model the development of bronchial epithelium. First, in vivo, teratomas were formed by the injection of hiPS into immunodeficient mice. Teratomas highlight the ability of differentiation of our hiPS into bronchial epithelium. Second, in vitro, reproducing embryonic and foetal bronchial development provides a way to model bronchial epithelium in a dish.These techniques open the door to many potential research avenues from screening small molecules to engineering stem cells to repair bronchial epithelium, and will in fine promote new pharmacologic or cell-based treatments for respiratory diseases. Ips Différenciation Épithélium bronchique Tératome Ips Differentiation Bronchus epithelium Teratoma
3	Hijacking Germ Cells for Cancer: Examining a 'Dead End' in Male Germ Cell Development Cook, Matthew Simon January 2010 (has links) <p>Germ cells represent the immortal line: they are guardians of a totipotent genome and are essential for the genetic survival of an individual organism and ultimately a species. An error at any stage in development (specification, migration, colonization, differentiation, adult maintenance) can lead to one of two disastrous outcomes: (1) germ cell death or (2) unchecked growth and proliferation leading to tumorigenesis. The work in this dissertation utilizes a classic mouse model (<italic>Ter</italic>) resulting in both of these phenotypes to further explore the molecular mechanisms important for development of germ cells. </p> <p>A homozygous nonsense mutation (<italic>Ter</italic>) in murine <italic>Dnd1</italic> (<italic>Dnd1<super>Ter/Ter</super></italic>) results in a significant (but not complete) early loss of primordial germ cells (PGCs) prior to colonization of the gonad in both sexes and all genetic backgrounds tested. The same mutation also leads to testicular teratomas only on the 129/SvJ background. Male mutants on other genetic backgrounds ultimately lose all PGCs with no incidence of teratoma formation. It is not clear how these PGCs are lost, develop into teratomas, or what factors directly control the strain-specific phenotype variation. </p> <p>Work here demonstrates that <italic>Dnd1</italic> expression is restricted to germ cells and that the <italic>Ter</italic> mutant defect is cell autonomous. The early loss of germ cells is due in part to BAX–mediated apoptosis which also affects the incidence of tumorigenesis on a mixed genetic background. Moreover, tumor formation is-specific to the male developmental pathway and not dependent on sex chromosome composition of the germ cell (XX vs. XY). Despite normal initiation of the male somatic pathway, mutant germ cells fail to differentiate as pro–spermatogonia and instead prematurely enter meiosis.</p> <p>Results here also reveal that, on a 129/SvJ background, many mutant germ cells fail to commit to the male differentiation pathway, instead maintain expression of the pluripotency markers, NANOG, SOX2, and OCT4, and initiate teratoma formation at the stage when male germ cells normally enter mitotic arrest. RNA immunoprecipitation experiments reveal that mouse DND1 directly binds a group of transcripts that encode negative regulators of the cell cycle, including <italic>p27Kip1</italic>, which is not translated in <italic>Dnd1<super>Ter/Ter</super></italic> germ cells. Additionally, overexpression of DND1 in a teratocarcinoma cell line leads to significant alteration of pathways controlling the G1/S checkpoint and the RB tumor suppressor protein. This strongly suggests that DND1 regulates mitotic arrest in male germ cells through regulation of cell cycle genes, serving as a gatekeeper to prevent the activation of a pluripotent program leading to teratoma formation. Furthermore, strain–specific morphological and expression level differences possibly account for sensitivity to tumor development.</p> / Dissertation Biology, Cell Developmental Biology Dead end germ cell RNA binding protein Ter teratoma
4	Benign Ovarian Tumors in Pregnancy: A Case Report of Metachronous Ipsilateral Recurrent Mucinous Cystadenoma in Initial Pregnancy and Mature Cystic Teratoma in Subsequent Pregnancy Schreck, Arielle M., Mikdachi, Hana F. 03 January 2019 (has links) Mucinous cystadenomas of the ovary are benign epithelial neoplasms that can grow rapidly during pregnancy. They may cause ovarian torsion, virilization, inferior vena cava syndrome, and even preterm labor and fetal growth restriction. Various theories exist regarding the pathogenesis of these tumors. One hypothesis suggests that they may arise from teratomas. Our case report describes synchronous mucinous cystadenomas and ovarian teratomas, as well as metachronous mucinous cystadenomas in patients with a history of ovarian teratoma. There has been no report of metachronous ipsilateral teratoma after previous mucinous cystadenoma. We present a 22-year-old female with a history of bilateral ovarian tumors in a prior pregnancy noted to have a recurrent ovarian mass on her left ovary at the time of cesarean section of a subsequent pregnancy. She had two prior cystectomies for metachronous mucinous cystadenomas of her left ovary, and a right salpingo-oophorectomy for the ovarian torsion in her previous pregnancy. On her current pregnancy, she developed a mature cystic teratoma of the remaining left ovary. The rapid growth and recurrence rate of these tumors highlights the importance of close surveillance of ovarian masses during pregnancy, even those that seem benign. In this case, a history of unilateral salpingo-oophorectomy with multiple contralateral cystectomies did not appear to affect her fertility. Her future ovarian reserve is unknown, pointing to the need for adequate pre-operative counseling in similar cases of ovarian masses in pregnancy. adnexal mass in pregnancy benign mature teratoma metachronous tumor mucinous cystadenoma synchronous tumor Obstetrics and Gynecology
5	A Novel Approach to Identify Candidate Imprinted Genes in Humans Shapiro, Jonathan 21 March 2012 (has links) Many imprinted genes are necessary for normal human development. Approximately 70 imprinted genes have been identified in humans. I developed a novel approach to identify candidate imprinted genes in humans using the premise that imprinted genes are often associated with nearby parent-of-origin-specific DNA differentially methylated regions (DMRs). I identified parent-of-origin-specific DMRs using sodium bisulfite-based DNA (CpG) methylation profiling of uniparental tissues, mature cystic ovarian teratoma (MCT) and androgenetic complete hydatidiform mole (AnCHM), and biparental tissues, blood and placenta. In support of this approach, the CpG methylation profiling led to the identification of parent-of-origin-specific differentially methylated CpG sites (DMCpGs) in known parent-of-origin-specific DMRs. I found new DMRs for known imprinted genes NAP1L5 and ZNF597. Most importantly, I discovered many new DMCpGs, which were associated with nearby genes, i.e., candidate imprinted genes. Allelic expression analyses of one candidate imprinted gene, AXL, suggested polymorphic imprinting of AXL in human blood. Allele Allele-specific DNA Methylation Allele-specific Gene Expression Allele-specific Expression Allele-specific Methylation AnCHM Androgenetic Androgenetic Mole Mole Complete Mole Hydatidiform Mole Complete Hydatidiform Mole Androgenetic Hydatidiform Mole Androgenetic Complete Hydatidiform Mole Biparental Tissue Bisulfite Bisulphite Blood Blood DNA Computational Biology DNA Methylation DNA Methylation Profiling Epigenetic Epi-genetic Epigenomic Epi-genomic Expression Expression Regulation Gene Expression Gene Expression Regulation Genetic Genetic Imprint Genetic Imprinting Genomic Genomic DNA Genomic Imprint Genomic Imprinting Human Imprint Imprinting Teratoma Ovarian Teratoma Cystic Teratoma Mature Teratoma Mature Cystic Teratoma Mature Ovarian Teratoma Cystic Ovarian Teratoma Mature Cystic Ovarian Teratoma MCT Methylation Cytosine Methylation Microarray Neoplasm Ovarian Neoplasm Placenta Profiling Promoter Promoter Region Sodium Bisulfite Sodium Bisulphite Uniparental Tissue WB WBC Imprinted Gene Polymorphic Imprinting Parent-of-origin Parent-of-origin-specific Methylation Parent-of-origin-specific Expression 0369 0307
6	A Novel Approach to Identify Candidate Imprinted Genes in Humans Shapiro, Jonathan 21 March 2012 (has links) Many imprinted genes are necessary for normal human development. Approximately 70 imprinted genes have been identified in humans. I developed a novel approach to identify candidate imprinted genes in humans using the premise that imprinted genes are often associated with nearby parent-of-origin-specific DNA differentially methylated regions (DMRs). I identified parent-of-origin-specific DMRs using sodium bisulfite-based DNA (CpG) methylation profiling of uniparental tissues, mature cystic ovarian teratoma (MCT) and androgenetic complete hydatidiform mole (AnCHM), and biparental tissues, blood and placenta. In support of this approach, the CpG methylation profiling led to the identification of parent-of-origin-specific differentially methylated CpG sites (DMCpGs) in known parent-of-origin-specific DMRs. I found new DMRs for known imprinted genes NAP1L5 and ZNF597. Most importantly, I discovered many new DMCpGs, which were associated with nearby genes, i.e., candidate imprinted genes. Allelic expression analyses of one candidate imprinted gene, AXL, suggested polymorphic imprinting of AXL in human blood. Allele Allele-specific DNA Methylation Allele-specific Gene Expression Allele-specific Expression Allele-specific Methylation AnCHM Androgenetic Androgenetic Mole Mole Complete Mole Hydatidiform Mole Complete Hydatidiform Mole Androgenetic Hydatidiform Mole Androgenetic Complete Hydatidiform Mole Biparental Tissue Bisulfite Bisulphite Blood Blood DNA Computational Biology DNA Methylation DNA Methylation Profiling Epigenetic Epi-genetic Epigenomic Epi-genomic Expression Expression Regulation Gene Expression Gene Expression Regulation Genetic Genetic Imprint Genetic Imprinting Genomic Genomic DNA Genomic Imprint Genomic Imprinting Human Imprint Imprinting Teratoma Ovarian Teratoma Cystic Teratoma Mature Teratoma Mature Cystic Teratoma Mature Ovarian Teratoma Cystic Ovarian Teratoma Mature Cystic Ovarian Teratoma MCT Methylation Cytosine Methylation Microarray Neoplasm Ovarian Neoplasm Placenta Profiling Promoter Promoter Region Sodium Bisulfite Sodium Bisulphite Uniparental Tissue WB WBC Imprinted Gene Polymorphic Imprinting Parent-of-origin Parent-of-origin-specific Methylation Parent-of-origin-specific Expression 0369 0307
7	La ventilation nasale du nouveau-né : études cliniques d'anomalies congénitales, modélisations numériques de l'écoulement et du réchauffement de l'air / Neonatal nasal breathing : clinical studies of congenital abnormalities, numerical modeling of airflow and air-conditioning Moreddu, Éric 07 December 2018 (has links) La ventilation nasale est vitale pour le nouveau-né, respirateur nasal exclusif. Le tiers antérieur des fosses nasales peut être modifié par une sténose congénitale de l’orifice piriforme, tandis leur partie postérieure peut être fermée par une atrésie choanale uni ou bilatérale ou par des lésions du nasopharynx.Les simulations numériques permettent d’analyser l’écoulement et le conditionnement de l’air en contournant les limites techniques et éthiques rencontrées in vivo. Devant la rareté des données dans la littérature, une étude de faisabilité a été nécessaire et concluante : les modèles numériques sont qualitativement proches de la réalité. Un travail sur les conditions physiologiques chez le nouveau-né a ensuite été réalisé, avec une méthodologie retravaillée. La reconstruction tridimensionnelle des fosses nasales est possible dès la naissance. La création d’une sphère centrée sur la pointe du nez, éloignant le domaine d’entrée de la zone d’intérêt, a permis d’analyser le rôle du tiers antérieur des fosses nasales.La valve nasale joue un rôle majeur en inspiration : perte de charge, accélération, guidage des flux et réchauffement de l’air. Les trois quarts du réchauffement ont lieu en amont du cornet inférieur. Une obstruction nasale entraîne une réduction des vitesses et une augmentation des températures de l'air. La simulation de l’inspiration d’air à 0°C a permis de constater que les fosses nasales permettent d’amortir les effets du refroidissement de l’air extérieur.Ce travail constitue une première approche de la physiologie de la ventilation nasale du nouveau-né par modélisation numérique, indispensable à la compréhension de la pathologie nasale néonatale. / Nasal breathing is essential for the newborn, exclusive nasal breather. The anterior third of the nasal fossae may be modified by a congenital stenosis of the pyriform aperture, while their posterior part may be closed by unilateral or bilateral choanal atresia.Numerical simulations are a good means to analyze airflow and air-conditioning: they circumvent the technical and ethical limits encountered in vivo. Given the rarity of available data in the literature, a feasibility study was necessary and was conclusive: numerical models are qualitatively close to reality. A work on the physiological conditions in newborns was conducted, using refined methodology. The three-dimensional reconstruction of the nasal fossae is possible from birth. The creation of a sphere centered on the tip of the nose, moving the boundary conditions away from the area of interest, made it possible to analyze the role of the anterior third od the nasal fossae.The nasal valve plays a major in inspiration: it is a zone of pressure loss, acceleration, flow guidance and air warming. Three-fourths of the warming takes place upstream the inferior turbinate. A partial nasal obstruction modifies these results with lower velocities and higher temperature of the air. The simulation of the inspiration of cold air (0°C) has shown that the nasal fossae can dampen, without canceling, the effects of air cooling. This work is a first approach to the physiology of nasal ventilation of the newborn by numerical modeling, which is essential to the understanding of neonatal nasal pathology. Voies aériennes Computational fluid dynamics Atrésie choanale Enfant Température Débits Obstruction nasale Rhinomanométrie Nez Fosses nasales Nouveau-Né Orifice piriforme Tératome Airway Computational fluid dynamics Choanal atresia Children Temperature Airflow Nasal obstruction Rhinomanometry Nose Nasal fossa Newborn Pyriform aperture Teratoma
8	Investigarion of Activated Phosphaidylinositol 3’ Kinase Signaling in Stem Cell Self-renewal and Tumorigenesis Ling, Ling 31 August 2012 (has links) The phosphatidylinositol 3' kinase (PI3K) pathway is involved in many cellular processes including cell proliferation, survival, and glucose transport, and is implicated in various disease states such as cancer and diabetes. Though there have been numerous studies dissecting the role of PI3K signaling in different cell types and disease models, the mechanism by which PI3K signaling regulates embryonic stem (ES) cell fate remains unclear. It is believed that in addition to proliferation and tumorigenicity, PI3K activity might also be important for self-renewal of ES cells. Paling et al. (2004) reported that the inhibition of PI3K led to a reduction in the ability of leukemia inhibitory factor (LIF) to maintain self-renewal causing cells to differentiate. Studies in our lab have revealed that ES cells completely lacking GSK-3 remain undifferentiated compared to wildtype ES cells. GSK-3 is negatively regulated by PI3K suggesting that PI3K may play a vital role in maintaining pluripotency in ES cells through GSK-3. By using a modified Flp recombinase system, we expressed activated alleles of PDK-1 and PKB to create stable, isogenic ES cell lines to further study the role of the PI3K signaling pathway in stem cell fate determination. In vitro characterization of the transgenic cell lines revealed a strong tendency towards maintenance of pluripotency, and this phenotype was found to be independent of canonical Wnt signal transduction. To assess growth and differentiation capacity in vivo, the ES cell lines were grown as subcutaneous teratomas. The constitutively active PDK-1 and PKB ES cell lines were able to form all three germ layers when grown in this manner – in contrast to ES cells engineered to lack GSK-3. The resulting PI3K pathway activated cells exhibited a higher growth rate which resulted in large teratomas. In summary, PI3K signaling is sufficient to maintain self-renewal and survival of stem cells. Since this pathway is frequently mutationally activated in cancers, its effect on suppressing differentiation may contribute to its oncogenicity. PI3K pathway PDK1 myr-PDK1 PKB PKB-DD GSK-3 p70S6K β-catenin Axin-2 Wnt pathway embyronic stem cells pluripotency self-renewal Oct-4 cell fate differentiation embryoid bodies teratoma formation tumorigenesis Akti-1/2 mTOR rapamycin endothelial cells vascularization proliferation apoptosis Flp-In system isogenic cell lines signal transduction myristoylation phosphomimetic 0307 0379
9	Investigarion of Activated Phosphaidylinositol 3’ Kinase Signaling in Stem Cell Self-renewal and Tumorigenesis Ling, Ling 31 August 2012 (has links) The phosphatidylinositol 3' kinase (PI3K) pathway is involved in many cellular processes including cell proliferation, survival, and glucose transport, and is implicated in various disease states such as cancer and diabetes. Though there have been numerous studies dissecting the role of PI3K signaling in different cell types and disease models, the mechanism by which PI3K signaling regulates embryonic stem (ES) cell fate remains unclear. It is believed that in addition to proliferation and tumorigenicity, PI3K activity might also be important for self-renewal of ES cells. Paling et al. (2004) reported that the inhibition of PI3K led to a reduction in the ability of leukemia inhibitory factor (LIF) to maintain self-renewal causing cells to differentiate. Studies in our lab have revealed that ES cells completely lacking GSK-3 remain undifferentiated compared to wildtype ES cells. GSK-3 is negatively regulated by PI3K suggesting that PI3K may play a vital role in maintaining pluripotency in ES cells through GSK-3. By using a modified Flp recombinase system, we expressed activated alleles of PDK-1 and PKB to create stable, isogenic ES cell lines to further study the role of the PI3K signaling pathway in stem cell fate determination. In vitro characterization of the transgenic cell lines revealed a strong tendency towards maintenance of pluripotency, and this phenotype was found to be independent of canonical Wnt signal transduction. To assess growth and differentiation capacity in vivo, the ES cell lines were grown as subcutaneous teratomas. The constitutively active PDK-1 and PKB ES cell lines were able to form all three germ layers when grown in this manner – in contrast to ES cells engineered to lack GSK-3. The resulting PI3K pathway activated cells exhibited a higher growth rate which resulted in large teratomas. In summary, PI3K signaling is sufficient to maintain self-renewal and survival of stem cells. Since this pathway is frequently mutationally activated in cancers, its effect on suppressing differentiation may contribute to its oncogenicity. PI3K pathway PDK1 myr-PDK1 PKB PKB-DD GSK-3 p70S6K β-catenin Axin-2 Wnt pathway embyronic stem cells pluripotency self-renewal Oct-4 cell fate differentiation embryoid bodies teratoma formation tumorigenesis Akti-1/2 mTOR rapamycin endothelial cells vascularization proliferation apoptosis Flp-In system isogenic cell lines signal transduction myristoylation phosphomimetic 0307 0379
10	Der Einfluss mechanischer Last auf das Potential multipotenter adulter Keimbahnstammzellen zur kardialen Regeneration / Influence of mechanical load on the cardiac regeneration potential of multipotent adult germline stem cells Kaiser, Diana 19 January 2011 (has links) No description available. 570 Biowissenschaften, Biologie Biology (incl. Psychology) maGSCs Stammzellen in vitro in vivo;TAC Shunt Maus Flk1 Kardiomyozyten Herz Myokard Differenzierung Regeneration Immunsytem Ciclosporin A Teratome maGSCs stem cells in vitri in vivo;TAC Shunt mouse Flk1 cardiomyocytes heart myocardium differentiation regeneration immune system Cyclosporine A teratoma 42

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