Academic literature on the topic 'Cell fat plasticity'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cell fat plasticity.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Cell fat plasticity"
1
Casteilla, Louis, Béatrice Cousin, and Mamen Carmona. "PPARs and Adipose Cell Plasticity." PPAR Research 2007 (2007): 1–7. http://dx.doi.org/10.1155/2007/68202.
Full textAbstract:
Due to the importance of fat tissues in both energy balance and in the associated disorders arising when such balance is not maintained, adipocyte differentiation has been extensively investigated in order to control and inhibit the enlargement of white adipose tissue. The ability of a cell to undergo adipocyte differentiation is one particular feature of all mesenchymal cells. Up until now, the peroxysome proliferator-activated receptor (PPAR) subtypes appear to be the keys and essential players capable of inducing and controlling adipocyte differentiation. In addition, it is now accepted that adipose cells present a broad plasticity that allows them to differentiate towards various mesodermal phenotypes. The role of PPARs in such plasticity is reviewed here, although no definite conclusion can yet be drawn. Many questions thus remain open concerning the definition of preadipocytes and the relative importance of PPARs in comparison to other master factors involved in the other mesodermal phenotypes.
2
Olson, Lorin E., and Philippe Soriano. "PDGFRβ Signaling Regulates Mural Cell Plasticity and Inhibits Fat Development." Developmental Cell 20, no. 6 (June 2011): 815–26. http://dx.doi.org/10.1016/j.devcel.2011.04.019.
Full text
3
Bielczyk-Maczynska, Ewa. "White Adipocyte Plasticity in Physiology and Disease." Cells 8, no. 12 (November 25, 2019): 1507. http://dx.doi.org/10.3390/cells8121507.
Full textAbstract:
Cellular plasticity is a transformation of a terminally differentiated cell into another cell type, which has been long known to occur in disease and regeneration. However, white adipocytes (fat cells) have only recently been observed to undergo different types of cellular plasticity. Adipocyte transdifferentiation into myofibroblasts and cancer-associated fibroblasts occurs in fibrosis and cancer, respectively. On the other hand, reversible adipocyte dedifferentiation into adipocyte progenitor cells (preadipocytes) has been demonstrated in mammary gland and in dermal adipose tissue. Here we discuss the research on adipocyte plasticity, including the experimental approaches that allowed to detect and study it, the current state of the knowledge, major research questions which remain to be addressed, and the advances required to stimulate adipocyte plasticity research. In the future, the knowledge of the molecular mechanisms of adipocyte plasticity can be utilized both to prevent adipocyte plasticity in disease and to stimulate it for use in regenerative medicine.
4
MOULIN, Karine, Nathalie TRUEL, Mireille ANDRÉ, Emmanuelle ARNAULD, Maryse NIBBELINK, Béatrice COUSIN, Christian DANI, Luc PÉNICAUD, and Louis CASTEILLA. "Emergence during development of the white-adipocyte cell phenotype is independent of the brown-adipocyte cell phenotype." Biochemical Journal 356, no. 2 (May 24, 2001): 659–64. http://dx.doi.org/10.1042/bj3560659.
Full textAbstract:
In mammals, two types of adipose tissue are present, brown and white. They develop sequentially, as brown fat occurs during late gestation whereas white fat grows mainly after birth. However, both tissues have been shown to have great plasticity. Thus an apparent transformation of brown fat into white fat takes place during post-natal development. This observation raises questions about a possible conversion of brown into white adipocytes during development, although indirect data argue against this hypothesis. To investigate such questions in vivo, we generated two types of transgenic line. The first carried a transgene expressing Cre recombinase specifically in brown adipocytes under the control of the rat UCP1 promoter. The second corresponded to an inactive lacZ gene under the control of the human cytomegalovirus promoter. This dormant gene is inducible by Cre because it contains a Stop sequence between two loxP sequences, separating the promoter from the coding sequence. Adipose tissues of progeny derived by crossing independent lines established from both constructs were investigated. LacZ mRNA corresponding to the activated reporter gene was easily detected in brown fat and not typically in white fat, even by reverse transcriptase PCR experiments. These data represent the first direct experimental proof that, during normal development, most white adipocytes do not derive from brown adipocytes.
5
Linehan, Victoria, Lisa Z. Fang, Matthew P. Parsons, and Michiru Hirasawa. "High-fat diet induces time-dependent synaptic plasticity of the lateral hypothalamus." Molecular Metabolism 36 (June 2020): 100977. http://dx.doi.org/10.1016/j.molmet.2020.100977.
Full text
6
Herzog, Erica L., Li Chai, and Diane S. Krause. "Plasticity of marrow-derived stem cells." Blood 102, no. 10 (November 15, 2003): 3483–93. http://dx.doi.org/10.1182/blood-2003-05-1664.
Full textAbstract:
AbstractBone marrow (BM) contains hematopoietic stem cells (HSCs), which differentiate into every type of mature blood cell; endothelial cell progenitors; and marrow stromal cells, also called mesenchymal stem cells (MSCs), which can differentiate into mature cells of multiple mesenchymal tissues including fat, bone, and cartilage. Recent findings indicate that adult BM also contains cells that can differentiate into additional mature, nonhematopoietic cells of multiple tissues including epithelial cells of the liver, kidney, lung, skin, gastrointestinal (GI) tract, and myocytes of heart and skeletal muscle. Experimental results obtained in vitro and in vivo are the subject of this review. The emphasis is on how these experiments were performed and under what conditions differentiation from bone marrow to epithelial and neural cells occurs. Questions arise regarding whether tissue injury is necessary for this differentiation and the mechanisms by which it occurs. We also consider which bone marrow subpopulations are capable of this differentiation. Only after we have a better understanding of the mechanisms involved and of the cells required for this differentiation will we be able to fully harness adult stem cell plasticity for clinical purposes. (Blood. 2003; 102:3483-3493)
7
De Fano, Michelatonio, Desirèe Bartolini, Cristina Tortoioli, Cristiana Vermigli, Massimo Malara, Francesco Galli, and Giuseppe Murdolo. "Adipose Tissue Plasticity in Response to Pathophysiological Cues: A Connecting Link between Obesity and Its Associated Comorbidities." International Journal of Molecular Sciences 23, no. 10 (May 14, 2022): 5511. http://dx.doi.org/10.3390/ijms23105511.
Full textAbstract:
Adipose tissue (AT) is a remarkably plastic and active organ with functional pleiotropism and high remodeling capacity. Although the expansion of fat mass, by definition, represents the hallmark of obesity, the dysregulation of the adipose organ emerges as the forefront of the link between adiposity and its associated metabolic and cardiovascular complications. The dysfunctional fat displays distinct biological signatures, which include enlarged fat cells, low-grade inflammation, impaired redox homeostasis, and cellular senescence. While these events are orchestrated in a cell-type, context-dependent and temporal manner, the failure of the adipose precursor cells to form new adipocytes appears to be the main instigator of the adipose dysregulation, which, ultimately, poses a deleterious milieu either by promoting ectopic lipid overspill in non-adipose targets (i.e., lipotoxicity) or by inducing an altered secretion of different adipose-derived hormones (i.e., adipokines and lipokines). This “adipocentric view” extends the previous “expandability hypothesis”, which implies a reduced plasticity of the adipose organ at the nexus between unhealthy fat expansion and the development of obesity-associated comorbidities. In this review, we will briefly summarize the potential mechanisms by which adaptive changes to variations of energy balance may impair adipose plasticity and promote fat organ dysfunction. We will also highlight the conundrum with the perturbation of the adipose microenvironment and the development of cardio-metabolic complications by focusing on adipose lipoxidation, inflammation and cellular senescence as a novel triad orchestrating the conspiracy to adipose dysfunction. Finally, we discuss the scientific rationale for proposing adipose organ plasticity as a target to curb/prevent adiposity-linked cardio-metabolic complications.
8
Rabhi, Nabil, and Stephen R. Farmer. "Unraveling the complexity of thermogenic remodeling of white fat reveals potential antiobesity therapies." Genes & Development 35, no. 21-22 (November 1, 2021): 1395–97. http://dx.doi.org/10.1101/gad.349053.121.
Full textAbstract:
Adipose tissue is a complex organ consisting of a mixture of mature adipocytes and stromal vascular cells. It displays a remarkable ability to adapt to environmental and dietary cues by changing its morphology and metabolic capacity. This plasticity is demonstrated by the emergence of interspersed thermogenic beige adipocytes within white depots in response to catecholamines secretion. Coordinated cellular interaction between different cell types within the tissue and a fine-tuned transcriptional program synergistically take place to promote beige remodeling. However, both cell–cell interactions and molecular mechanisms governing beige adipocyte appearance and maintenance are poorly understood. In this and the previous issue of Genes & Development, Shao and colleagues (pp. 1461–1474) and Shan and colleagues (pp. 1333–1338) advance our understanding of these issues and, in doing so, highlight potential therapeutic strategies to combat obesity-associated diseases.
9
Petan, Toni, Eva Jarc, and Maida Jusović. "Lipid Droplets in Cancer: Guardians of Fat in a Stressful World." Molecules 23, no. 8 (August 3, 2018): 1941. http://dx.doi.org/10.3390/molecules23081941.
Full textAbstract:
Cancer cells possess remarkable abilities to adapt to adverse environmental conditions. Their survival during severe nutrient and oxidative stress depends on their capacity to acquire extracellular lipids and the plasticity of their mechanisms for intracellular lipid synthesis, mobilisation, and recycling. Lipid droplets, cytosolic fat storage organelles present in most cells from yeast to men, are emerging as major regulators of lipid metabolism, trafficking, and signalling in various cells and tissues exposed to stress. Their biogenesis is induced by nutrient and oxidative stress and they accumulate in various cancers. Lipid droplets act as switches that coordinate lipid trafficking and consumption for different purposes in the cell, such as energy production, protection against oxidative stress or membrane biogenesis during rapid cell growth. They sequester toxic lipids, such as fatty acids, cholesterol and ceramides, thereby preventing lipotoxic cell damage and engage in a complex relationship with autophagy. Here, we focus on the emerging mechanisms of stress-induced lipid droplet biogenesis; their roles during nutrient, lipotoxic, and oxidative stress; and the relationship between lipid droplets and autophagy. The recently discovered principles of lipid droplet biology can improve our understanding of the mechanisms that govern cancer cell adaptability and resilience to stress.
10
Baragetti, Andrea, and Giuseppe Danilo Norata. "The High Fat Diet Impacts the Plasticity between Fresh and Aged Neutrophils." Journal of Cellular Immunology 5, no. 5 (2023): 168–73. http://dx.doi.org/10.33696/immunology.5.182.
Full textAbstract:
Metabolic alterations induced by unhealthy lifestyles, including obesity and insulin resistance are often associated with increased innate immune response and chronic inflammation. Cholesterol has been identified as a key metabolite driving the activation of the inflammasome and the “epigenetic memory” in long-term living hematopoietic stem cells. In addition to these mechanisms, the physiological aging of short-living neutrophils is a relevant modifier of their immune competency, as while they egress from medullary niches as “fresh”, fully competent, cells, they turn into “aged”, disarmed cells, when they extravasate into peripheral tissues to fight against pathogens or they reach the spleen for disposal. We recently observed that cardio-metabolic alterations induced by a lipid enriched unhealthy diet critically accelerate this process. Indeed, the chronic feeding with a high fat diet (HFD) results in the increase of aged neutrophils in the circulation and their accumulation in liver. This profile is associated with a deteriorated insulin response and obesity. The HFD primes aged, but not fresh neutrophils, to infiltrate in the liver and promotes inflammation coupled to altered cell immune architecture in visceral adipose tissue. Preventing the aging of neutrophils via selective ablation of CXCR2, reduces the development of obesity and improves the sensitivity to insulin. In humans, plasma levels of CXCL1, one of the cytokines binding CXCR2 and promoting neutrophil aging, are directly associated with abdominal adiposity and fatty liver independently of other risk factors. Together these findings point to a direct role of aged neutrophils in the development of metabolic disorders.
Dissertations / Theses on the topic "Cell fat plasticity"
1
Caldarelli, Paolo. "On the role of mechanical forces in embryonic self-organization." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS189.
Full textAbstract:
Les cellules se divisent, migrent, se réarrangent et acquièrent différents destins au cours du développement embryonnaire tout en s'organisant de manière à constituer un organisme de forme adéquate. Il est de plus en plus reconnu que la régulation de ces événements est contrôlée par des mécanismes d'auto-organisation. À la suite des travaux pionniers d'Alan Turing, qui a postulé, dans son modèle de réaction-diffusion, que l'interaction entre les molécules pouvait contrôler l'auto-organisation, des études ultérieures se sont concentrées sur l'identification des molécules de signalisation répondant aux critères de Turing. Cependant, alors que les forces mécaniques sont générées et propagées à l'échelle des tissus au cours de la morphogenèse, la possibilité qu'elles puissent agir comme des signaux dans l'auto-organisation embryonnaire est largement sous-explorée. L'embryon aviaire au stade de gastrula, qui se prête bien aux approches d'imagerie sur embryon vivant et aux perturbations mécaniques, constitue un excellent modèle pour étudier le rôle des forces mécaniques au cours du développement. En outre, les expériences classiques ont démontré la nature hautement régulatrice et auto-organisée du développement précoce des oiseaux : lorsque le disque épithélial précoce (blastoderme) est divisé en deux, des embryons entièrement formés émergent de chaque partie séparée. Bien que des travaux récents effectués au laboratoire aient permis de dresser un tableau précis des mécanismes qui façonnent l'embryon à ce stade, leur rôle dans la régulation et l'auto-organisation de l'embryon reste à étudier, et c'est précisément le sujet de cette thèse de doctorat. En collaboration avec un physicien, nous avons tout d'abord formulé un modèle mathématique qui rend compte de l’état stable des forces observées à la marge entre la région embryonnaire et extra-embryonnaire de l'embryon. Ce modèle est fondé sur l'hypothèse que la mécanique tissulaire à la marge s'auto-organise par analogie à un système mécanique de Turing : la contractilité tissulaire agit comme un activateur local et la tension tissulaire comme un inhibiteur à longue portée. Nous avons obtenu des prédictions novatrices, que nous avons testées expérimentalement pour évaluer la validité de notre modèle et, plus généralement, pour explorer le lien entre les forces mécaniques et l'expression génétique. Nous avons constaté que la modulation de la contractilité des tissus à la marge modifie l'expression normale de Gdf1, un morphogène clé dans la formation de l'embryon, et entraîne la formation de lignes primitives ectopiques (axe primaire du corps). Nous avons ensuite perturbé l'embryon mécaniquement. En utilisant l'imagerie sur embryon vivant et l'ablation au laser, nous avons pu orienter et bissecter précisément le blastoderme précoce. Nous avons constaté que dans les moitiés antérieures, la contractilité des tissus peut déclencher de manière ectopique l'expression de Gdf1 et la formation de lignes primitives. Par la suite, pour explorer davantage la rétroaction entre la mécanique des tissus et l'expression des gènes, nous nous sommes concentrés sur la moitié bissectée postérieure où Gdf1 est exprimé de manière endogène. Nous avons montré qu'après quelques heures suivant la coupe, les forces mécaniques se redimensionnent en fonction de la nouvelle taille de la marge et des domaines d'expression de Gdf1. De plus, nous avons également constaté que l'expression de certains marqueurs des territoires embryonnaires suivent le redimensionnement de la marge, suggérant un rôle actif de la mécanique tissulaire dans l'allocation du destin cellulaire au cours du développement. Enfin, nous avons montré que des lignes primitives ectopiques pouvaient se former en plaçant un obstacle physique à la marge, suivant une prédiction selon laquelle une friction ectopique s'ajoute au mouvement du tissu à la marge. [...]During embryonic development, cells divide, migrate, rearrange, acquire different fates while organizing into a properly shaped organism. The regulation of these events is increasingly recognized to be controlled by self-organizing mechanisms. Following the seminal work of Alan Turing, who postulated, in his reaction-diffusion model, that self-organization could be controlled by the interaction between molecules, subsequent studies have focused on the identification of signaling molecules fulfilling Turing’s criteria. However, mechanical forces are generated and propagated at the tissue-scale level during morphogenesis, yet the possibility that they might act as signals in embryonic self-organization is largely underexplored. The gastrulating avian embryo, which is highly amenable to both live imaging approaches and mechanical perturbations, represents a great model to investigate the role of mechanical forces during development. Furthermore, classic experiments have demonstrated the highly regulative and self-organizing nature of early avian development: when the early epithelial disk (blastoderm) is bisected, fully formed embryos emerge from each separated part. Although recent work performed in the lab has drawn a precise mechanical picture that shapes the embryo at this stage, their role in regulating and self-organizing the embryo remains elusive, and it is the subject of this Ph.D. thesis. In collaboration with a physicist, we first formulated a mathematical model that accounts for the steady pattern of forces observed at the margin between the embryonic and extraembryonic region of the embryo. The model is based on the hypothesis that tissue mechanics at the margin self-organizes in analogy to a mechanical Turing system: tissue contractility acts as a local activator and tissue tension as a long-range inhibitor. We obtained unique predictions, which we tested experimentally to validate our model and ultimately explore the link between mechanical forces and gene expression. We found that modulation of tissue contractility at the margin alters the normal expression of Gdf1, a key morphogen in the formation of the embryo, and results in the formation of ectopic primitive streaks (primary body axis). We then perturbed the embryo mechanically. Using time-lapse imaging and laser ablation, we could orient and precisely bisect the early blastoderm. We found that in anterior halves, tissue contractility can ectopically initiate Gdf1 expression and primitive streak formation. Subsequently, to further explore the feedback between tissue mechanics and gene expression, we focused on the posterior bisected half where Gdf1 is endogenously expressed. We showed that after a few hours from the cut, the mechanical forces rescale according to the new size of the margin along with the expression domains of Gdf1. Moreover, we also found that the expression of selected embryonic territories markers follows the rescaling of the margin, suggesting an active role of tissue mechanics in allocating cell fate during development. Lastly, we showed that ectopic primitive streaks could form by placing a physical obstacle at the margin, following a prediction whereby ectopic friction is added to the motion of the tissue at the margin. This last result strongly argues against molecular diffusion as the driver of self-organization and rules out spurious events in the formation of ectopic embryos upon bisection (i.d. wound healing). Thus, this work uncovers the role of mechanical forces as signaling factors during embryonic development and demonstrates that tissue mechanics at the margin of the embryo self-organizes and underlies embryonic regulation in amniotes
2
Eid, André. "Mechanisms of cell fate and chromatin plasticity during early mouse embryogenesis." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ014/document.
Full textAbstract:
La chromatine embryonnaire subit des changements nécessaires pour l’établissement d’un nouveau programme développemental. Ce travail a étudié l’organisation de l’hétérochromatine au cours du développement sous trois facettes. La première étant celle de d’hétérochromatine constitutive, à travers, l’établissement forcé de la marque H4K20me3 qui provoque un arrêt du développement préimplantatoire. Ce phénotype dépend spécifiquement de l’activité de la methyltransferase SUV4-20h2 et induit l’activation de la voie de signalisation ATR qui bloque la phase de réplication. En deuxième partie, l’hétérochromatine facultative a été le sujet d’une analyse de l’expression des protéines du complexe non-canonique PRC1 et de la modification H2AK119ub qui en résulte. Finalement, une analyse de la chromatine embryonnaire a été mise en place et a permis la détection des changements de niveau de compaction au cours du développement préimplantatoireEmbryonic chromatin undergoes necessary changes to establish a new developmental program. This work has addressed the organization of heterochromatin in preimplantation embryos from three angles. The first part probed the absence of constitutive heterochromatin by forcing the establishment of the H4K20me3 mark which results in an embryonic arrest prior to the 2-cell stage. This phenotype is due to the specific histone methyl-transferase activity of SUV4-20h2 and is induced by ATR activation which blocks replication. In the second part, facultative heterochromatin was studied by analyzing the levels of several members of the non-canonical PRC1 complex as well as the resultant modification H2AK119ub. Finally, an analysis of the embryonic chromatin was set up and allowed for the measurement of changes in the chromatin openness during preimplantation development
3
André-Ratsimbazafy, Marie. "Phenotype plasticity and populations’ dynamics : social interactions among cancer cells." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB032/document.
Full textAbstract:
On admet communément que les tumeurs proviennent de cellules échappant aux contrôles homéostatiques qui sous-tendent les structures histologiques saines et que le phénotype d’une cellule n’est pas le résultat de processus génétiques et biochimiques déterministes mais la conséquence stochastique de réseaux de régulation intra- et intercellulaires. Ce doctorat vise à étudier quantitativement l’homéostasie phénotypique de populations cellulaires et à présenter une approche à la question fondamentale, mais jusqu’alors jamais étudiée, concernant l’autonomie versus le contrôle collectif du devenir des cellules. Nous avons étudié sur le long terme, par cytométrie de flux et dans des conditions 2D puis 3D, le niveau d’expression de CD24 et CD44 de deux lignées cellulaires de cancer du sein (SUM149-PT et SUM159-PT). Trois phénotypes ont été isolés (CD24-/CD44+, CD24+/CD44+, CD24-/CD44-), ce dernier n’avait pour le moment pas été documenté dans la littérature. Le comportement phénotypique des sous-populations CD44-low et CD44-high a été caractérisé en évaluant leur proportion et en analysant leur spectre de fluorescence. Ainsi nous avons observé des comportements périodiques d’apparition et de disparition de pool de cellules caractéristiques des lignées et une re-diversification des phénotypes pour chacune des sous-population. Seule la population issue de CD24-/CD44- re-diversifiée présente le même équilibre que la population initiale non triée. En 3D, le processus de re-diversification a été observé dans les tumorsphères issues de CD24-/CD44+ et CD24+/CD44+. Les cellules CD24-/CD44- n’ont pas ce potentiel mais survivent néanmoins à l’anoïkis. Ces comportements laissent penser qu’il existe une coordination intercellulaire régulant l’équilibre des proportions phénotypiques. Pour découvrir les règles sociales régissant l’organisation spatiale inter-phénotypique, nous avons mis en place un rapporteur des variations du niveau d’expression endogène des marqueurs d’intérêt et élaboré un modèle théorique d’interactions cellulaires. Ce travail a conforté notre hypothèse selon laquelle il s’établit des règles sociales inter-cellulaires déterminant l’expression phénotypique à l’échelle uni- et pluricellulaireIt is commonly accepted that tumors arise from cells that escape the homeostatic controls which underlie the healthy histological structure and that cell phenotype is not the result of deterministic biochemical and genetic processes, but rather the stochastic and dynamic outcome of multiple intra- and intercellular regulation networks. This PhD aims to quantitatively study the phenotypic homeostasis of the cell populations and to present an approach to the fundamental question, never heretofore studied, regarding the autonomy versus collective control of cell fate. We studied in the long run, using flow cytometry and in 2D and 3D conditions, the level of expression of CD24 and CD44 of two breast cancer cell lines (SUM149-PT and SUM159-PT). Three phenotypes were isolated (CD24-/CD44+, CD24+/CD44+, CD24-/CD44-), the latter had not previously been documented in the literature. The phenotypic behavior of CD44-low and CD44-high subpopulations has been characterized by assessing their proportion and analyzing the fluorescence map. Thereby, we observed both a periodic behavior of appearance and disappearance of pool of cells characteristics of each cell lines and a phenotypic re-diversification for each subpopulation. Only the resulting population derived from CD24-/CD44- provided the same balance as the original unsorted population. 3D re-diversification process was observed in tumorspheres from CD24-/CD44+ and CD24+/CD44+. The cells CD24-/CD44did not have that potential but nonetheless outlived anoikis. These behaviors suggest that there is an inter-cell coordination regulating the balance of phenotypic proportions. To discover the social rules regulating inter-phenotypic spatial organization, we have set up a reporter of the endogenous variations of CD24 and CD44 and developed a theoretical model of cell interactions. This work has confirmed our hypothesis that inter-cellular social rules are determining the phenotypic expression at both the uni- and multicellular scales
4
Son, Yesde. "Exploring the Plasticity of Cellular Fate Using Defined-Factor Reprogramming." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10309.
Full textAbstract:
Cellular fate, once established, is usually stable for the lifetime of the cell. However, the mechanisms that restrict the developmental potential of differentiated cells are in principle reversible, as demonstrated by the success of animal cloning from a somatic genome through somatic cell nuclear transfer (SCNT). An increased understanding of the molecular determinants of cell fate has also enabled the reprogramming of cell fate using defined transcription factors; recently, these efforts have culminated in the discovery of four genes that convert somatic cells into induced pluripotent stem cells (iPSCs), which resemble embryonic stem cells (ESCs) and can give rise to all the cell types in the body. As a first step toward generating clinically useful iPSCs, we identified a small molecule, RepSox, that potently and simultaneously replaces two of the four exogenous reprogramming factors, Sox2 and cMyc. This activity was mediated by the inhibition of the Transforming Growth Factor-\(\beta\) \((Tgf-\beta)\) signaling pathway in incompletely reprogrammed intermediate cells. By isolating these stable intermediates, we showed that RepSox acts on them to rapidly upregulate the endogenous pluripotency factor, Nanog, allowing full reprogramming to pluripotency in the absence of Sox2. We also explored lineage conversion as an alternative approach for producing a target cell type in a patient-specific manner, without first generating iPSCs. A combination of pro-neural as well as motor neuron-selective factors could convert fibroblasts directly into spinal motor neurons, the cells that control all voluntary movement. The induced motor neurons (iMNs) displayed molecular and functional characteristics of bona fide motor neurons, actuating muscle contraction in vitro and even engrafting in the developing chick spinal cord when transplanted. Importantly, functional iMNs could be produced from fibroblasts of adult patients with the fatal motor neuron disease, amyotrophic lateral sclerosis (ALS). Given the therapeutic value of generating patient-specific cell types on demand, defined-factor reprogramming is likely to serve as an important tool in regenerative medicine. It is hoped that the different approaches presented here can complement existing technologies to facilitate the study and treatment of intractable human disorders.
5
Saiz, Nestor. "Regulation of cell fate and cell behaviour during primitive endoderm formation in the early mouse embryo." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/regulation-of-cell-fate-and-cell-behaviour-during-primitive-endoderm-formation-in-the-early-mouse-embryo(d40bb786-85ed-4efd-af64-aab331df98e8).html.
Full textAbstract:
The preimplantation stages of mammalian development are dedicated to the differentiation of two extraembryonic epithelia, the trophectoderm (TE) and the primitive endoderm (PrE), and their segregation from the pluripotent embryonic lineage, the epiblast. The TE and PrE are responsible for implantation into the uterus and for producing the tissues that will support and pattern the epiblast as it develops into the foetus. PrE and epiblast are formed in a two step process that involves random cell fate specification, mediated by fibroblast growth factor (FGF) signalling, and cell sorting through several mechanisms. In the present work I have addressed aspects of both steps of this process. Chimaera assays showed that epiblast precursors transplanted onto a recipient embryo rarely differentiate into PrE, while PrE precursors are able to switch their identity and become epiblast. Transient stimulation or inhibition of the FGF4-ERK pathway in the chimaeras can modify the behaviour of these cells and restore the plasticity of epiblast precursors. This work shows that epiblast precursors are refractory to differentiation signals, thus ensuring the preservation of the embryonic lineage. I have also found that atypical Protein Kinase C (aPKC) is a marker of PrE cells and that pharmacological inhibition of aPKC impairs the segregation of PrE and epiblast precursors. Furthermore, it affects the survival of PrE cells and can alter the subcellular localisation of the PrE transcription factor GATA4. These data indicate aPKC plays a central role for the sorting of the PrE and epiblast populations and links cell position within the embryo to PrE maturation and survival. Lastly, I have found that aPKC can directly phosphorylate GATA4 in vitro. Knockdown of GATA4 affects cell position within the embryo, whereas aPKC knockdown reduces the number of GATA4-positive cells. These results indicate GATA4 plays an important role in cell sorting during preimplantation development and suggest phosphorylation by aPKC could determine its presence in the nuclei of PrE cells. My work, in the light of the current knowledge, supports a model where the earliest cell fate decisions during mammalian development depend on cellular interactions and not on inherited cell fate determinants. This robust mode of development underlies the plasticity of the preimplantation embryo and ensures the formation of the first mammalian cell lineages, critical for any further progression in mammalian development.
6
Flici, Hakima. "Différenciation et plasticité des cellules souches neurales." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-01070644.
Full textAbstract:
L'étude de la plasticité cellulaire est un puissant outil pour comprendre le choix du destin cellulaire pendant la différenciation et dans les processus cancéreux lors de la transformation d'une cellule normale en une cellule maligne. Chez la drosophile, le facteur de transcription Gcm contrôle la détermination du destin glial. Dans des mutants gcm, les cellules qui se développent normalement en glie entrent dans la voie de différenciation neuronale alors que l'expression ectopique de gcm dans des progéniteurs neuronaux induit de la glie. Ces données font de Gcm un outil important pour comprendre les bases de la plasticité cellulaire. Mon projet de thèse vise à comprendre les mécanismes contrôlant la plasticité des cellules souches neurales. Nous avons ainsi montré que la capacité des CSNs à se convertir en glie après expression forcée de Glide/Gcm décline avec l'âge et que lors de l'entrée en phase quiescente ou apoptotique, ils ne peuvent plus être convertis. Nous avons aussi découvert que le processus de conversion du destin ne se manifeste pas uniquement par l'expression de marqueurs gliaux mais aussi par des changements spécifiques au niveau de la chromatine. D'une manière intéressante, nous avons aussi montré que la stabilité de la protéine Glide/Gcm est contrôlée par deux voies opposées, où Repo et l'histone acetyltransférase CBP jouent un rôle majeur.
7
Jarjour, Meryem. "Plasticité des réseaux de cellules folliculaires dentritiques : Développement & remodelage." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM4014.
Full textAbstract:
Les Cellules Folliculaires Dendritiques (FDC) régulent l'homéostasie des lymphocytes B et sont indispensables à la mise en place des réponses immunes humorales. Les FDC s'organisent, au sein des organes lymphoïdes secondaires, en réseaux tridimensionnels denses, nécessaires à leur fonctionnement. Les études s'intéressant aux FDCs, empruntent classiquement des approches in vitro ou ex vivo, peu adaptées à la nature de ce type cellulaire. Au cours de mon travail de thèse, nous avons utilisé plusieurs systèmes de 'multicolor fate mapping' dans le but de déchiffrer in situ les mécanismes à l'origine du développement initial, et du remodelage des réseaux de FDCs en contexte inflammatoire. Nous avons démontré que les FDCs provenaient de la prolifération clonale et de la différentiation des Cellules Marginales Réticulaires (MRC), un autre sous-type cellulaire stromal résidant près des sinus sous-capsulaires ganglionnaires, et dont les fonctions étaient à ce jour, inconnues. Lors des réponses immunes, nous avons prouvé que les FDCs nouvellement formées, ne dérivaient ni du recrutement de progéniteurs circulants ni de la prolifération de FDCs matures, mais plutôt de la prolifération clonale des MRCs, suivie de leur différentiation en FDCs. Au-delà de l'étude de la biologie des FDCs, notre travail a révélé une fonction importante des MRCs dans le soutien de la plasticité des réseaux de FDCsFollicular Dendritic Cells (FDCs) regulate B cell function and development of high affinity antibody responses but little is known about their biology. FDCs associate in intricate cellular networks within secondary lymphoid organs. In vitro and ex vivo methods may thus be of little interest to understand the genuine immunobiology of FDCs in their native habitat. Herein, we utilised various multicolor fate mapping systems to investigate the ontogeny and dynamics of lymph node (LN) FDCs in situ. We show that LN FDC networks arise from the clonal expansion and differentiation of Marginal Reticular Cells (MRCs), a population of lymphoid stromal cells lining the LN subcapsular sinus. We further demonstrate that during an immune response, FDCs accumulate in germinal centers and that neither the recruitment of circulating progenitors nor the division of local mature FDCs significantly contributes to this accumulation. In contrast, we provide evidence that newly generated FDCs also arise from the proliferation and differentiation of MRCs, thus unraveling a critical function of this poorly defined stromal cell population
8
Polgárová, Kamila. "Diferenciační plasticita hematopoetických buněk." Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-404420.
Full textAbstract:
Hematopoiesis has been for many years seen as a straightforward process based on sequential restriction of cell fate potential leading to production of mature blood cells. In the last decade, however, several works documented an unexpected plasticity of hematopoietic cells with expanded potential of myeloid development from lymphoid progenitors and vice versa. Under physiologic conditions hematopoiesis is tightly controlled and the definite cell fate is denominated by multiple factors that all lead to changes in regulatory networks that include transcription factors, epigenetic changes and post-transcriptional modulations. Any disruption of this strict regulation, caused by mutations or other events, affects the proliferation and lineage fidelity of hematopoietic precursors. This may lead to clonal growth of variable significance or leukemogenesis and may possibly affect the treatment sensitivity of the hematological malignancies. For better understanding of hematopoietic regulation we described gene expression changes during physiological development of lymphoid and myeloid lineages and in leukemic specimens using our own simplified real-time PCR based platform. We investigated expression of 95 genes connected with lymphoid and myeloid differentiation or with leukemogenesis in sorted hematopoietic...
9
Patel, Tulsi. "Cell fate restriction in Caenorhabditis elegans is orchestrated by precise chromatin organization and transcription factor activity." Thesis, 2016. https://doi.org/10.7916/D8H1321F.
Full textAbstract:
The plasticity of cells in a multicellular organism is progressively lost during differentiation. This loss is reflected in studies involving the ectopic misexpression of fate-specifying or terminal selector transcription factors (TFs). These TFs can efficiently activate target genes in undifferentiated cells, but lose this ability as cells differentiate. While this phenomenon of cell fate restriction is widely observed, the mechanisms orchestrating it are poorly understood. In this thesis, I have used the ubiquitous overexpression of Zn-finger-TF CHE-1 as a tool to understand the mechanisms that restrict cell fate in Caenorhabditis elegans. When CHE-1 is ubiquitously expressed at embryonic stages, it activates target gene expression in many cell types, while in adults it can only act in a few neurons. To uncover factors that inhibit plasticity of all other adult cells, I first performed an RNAi screen against chromatin-associated factors. Using this approach I found that the removal of either the PRC2 complex, which deposits the H3K27me3 mark, or loss of proteins that indirectly regulate domains of H3K27me3, allows CHE-1 and two other terminal selector TFs to activate target genes in the germline. These data show that the correct distribution of H3K27me3 is crucial for the restriction of germ cell fate. I next took a candidate approach to identify genes that regulate fate restriction in other cell types. We hypothesized that terminal selector TFs themselves, in addition to specifying cellular identity by controlling large gene sets, may also act to inhibit plasticity. To test this, I first assayed the activity of CHE-1 in mutants of COE-TF unc-3, the terminal selector for a subset of cholinergic motor neurons (MNs). I found that in contrast to wildtype MNs, unc-3 mutant MNs remain plastic as CHE-1 can induce expression of target genes in these cells even at the adult stage. This phenotype is also observed in four of six additional terminal selector mutants tested. I further found that the removal of met-2, a protein required for H3K9 methylation, or mes-2, a PRC2 component, also makes differentiated cholinergic MNs amenable to the activity of CHE-1. Preliminary evidence suggests that met-2 may act in the same pathway as unc-3. These results raise the exciting possibility that selector TFs play a role in restricting cell fate by organizing the heterochromatin domains in differentiated cells. Overall, in this work I provide functional evidence to show that specific chromatin-modifying enzymes restrict the fate of germ cells and that both fate-specifying TFs and chromatin-modifying enzymes are required for the fate restriction in neurons.
Book chapters on the topic "Cell fat plasticity"
1
Dani, Christian. "Fat Cell Progenitors: Origins and Plasticity." In Research and Perspectives in Endocrine Interactions, 77–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13517-0_7.
Full text
2
Jiang, Jinxia, Min Feng, Annemarie Jacob, Lin Z. Li, and He N. Xu. "Optical Redox Imaging Differentiates Triple-Negative Breast Cancer Subtypes." In Advances in Experimental Medicine and Biology, 253–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_40.
Full textAbstract:
AbstractTriple-negative breast cancer (TNBC) is a highly diverse group of cancers with limited treatment options, responsible for about 15% of all breast cancers. TNBC cells differ from each other in many ways such as gene expression, metabolic activity, tumorigenicity, and invasiveness. Recently, many research and clinical efforts have focused on metabolically targeted therapy for TNBC. Metabolic characterization of TNBC cell lines can facilitate the assessment of therapeutic effects and assist in metabolic drug development. Herein, we used optical redox imaging (ORI) techniques to characterize TNBC subtypes metabolically. We found that various TNBC cell lines had differing redox statuses (levels of reduced nicotinamide adenine dinucleotide (NADH), oxidized flavin adenine dinucleotide (FAD), and the redox ratio (FAD/(NADH+FAD)). We then metabolically perturbed the cells with mitochondrial inhibitors and an uncoupler and performed ORI accordingly. As expected, we observed that these TNBC cell lines had similar response patterns to the metabolic perturbations. However, they exhibited differing redox plasticity. These results suggest that subtypes of TNBC cells are different metabolically and that ORI can serve as a sensitive technique for the metabolic profiling of TNBC cells.
3
Cinti, Saverio. "The Nutritional System." In Perspectives in Nursing Management and Care for Older Adults, 215–24. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63892-4_17.
Full textAbstract:
AbstractThe white and brown adipose tissues are organized to form a true organ. They have a different anatomy and perform different functions, but they collaborate thanks to their ability to convert mutually and reversibly following physiological stimuli. This implies a new fundamental property for mature cells, which would be able to reversibly reprogram their genome under physiological conditions. The subcutaneous mammary gland provides another example of their plasticity. Here fat cells are reversibly transformed into glands during pregnancy and breastfeeding. The obese adipose organ is inflamed because hypertrophic fat cells, typical of this condition, die and their cellular residues must be reabsorbed by macrophages. The molecules produced by these cells during their reabsorption work interfere with the insulin receptor, and this induces insulin resistance, which ultimately causes type 2 diabetes. The adipose organ collaborates with those of digestion. Both produce hormones that can influence the nutritional behavior of individuals. They produce molecules that mutually influence functional activities including thermogenesis, which contributes to the interruption of the meal. The nutrients are absorbed by the intestine, stored in the adipose organ, and distributed by them to the whole body between meals. Distribution includes offspring during breastfeeding. The system as a whole is therefore called the nutritional system.
4
Kokai, Lauren, and J. Peter Rubin. "Plastic surgery, fat, and fat plasticity: How adipose tissue changed the landscape of stem cell therapeutics." In Scientific Principles of Adipose Stem Cells, 3–8. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-819376-1.00009-3.
Full text
5
Wolf, Jason B., Edmund D. Brodie, and Michael J. Wade. "The Genotype-Environment Interaction and Evolution When the Environment Contains Genes." In Phenotypic Plasticity, 173–90. Oxford University PressNew York, NY, 2004. http://dx.doi.org/10.1093/oso/9780195138962.003.0011.
Full textAbstract:
Abstract The context in which genes are expressed is often a major determinant of the phenotype (including fitness) associated with a given genotype (Schlichting and Pigliucci 1998; Wolf et al. 2000; chapter I). Contexts that influence genetic effects span a hierarchy that begins within the cell and extends beyond the individual as far as the ecological community. Below the level of the individual, such context dependence is called epistasis, wherein the genetic background provided by other loci influences the effect that a given locus has on the phenotype. Epistasis may also arise when the cytoplasmic environment, provided by organelles such as mitochondria, influences the expression of nuclear genes and vice versa. Beyond the individual, we often think of genotype-environment interaction (GxE) as a result of interactions between the genotype and the context deriving from the abiotic ecological environment. But other contexts include the environment provided by conspecifics in social interactions (e.g., Wade 1980; Moore et al. 1997; Brodie 2000; Wolf 2000) and by other species in community interactions (e.g., Wade 1990; Goodnight 1991 ). Although the tools and perspective of plasticity and GxE research can help us understand the general phenomenon of context-dependent expression, they often ignore the fact that many, if not most, of the ecologically relevant contexts are themselves genetically determined.
6
Engleka, Kurt A., Deborah Lang, Christopher B. Brown, Nicole B. Antonucci,, and Jonathan A. Epstein. "Neural Crest Formation and Craniofacial Development." In Inborn Errors Of Development, 69–78. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0006.
Full textAbstract:
Abstract Neural crest describes a transitory group of pluripotent epithelial cells that originates from the dorsalmost ridges of the embryonic neural tube. During early development, many of these cells collectively transform to a mesenchymal phenotype, assuming new morphological characteristics distinct from their epithelial neighbors, segregate from the neural tube and stream through speci7c routes into neighboring tissue environments in a wave of proliferation and migration. The resultant cells spread along migratory pathways that may end relatively far from the neural tube of origin. They ultimately differentiate into a plethora of cells and tissues, a step coinciding with the cessation of cellular growth and movement. Neural crest is an apparent vertebrate innovation. It serves as a major cellular source for much of the head and face and peripheral nervous system and forms derivatives as diverse as neurons in the gastrointestinal tract, pigment cells in the skin, hair and inner ear, adrenomedullary cells and smooth muscle in the cardiac outMow tract. The proliferation, migration, and plasticity displayed by neural crest cells are distinctive relative to primary germ layers and other early embryonic cell populations. Abnormalities in neural crest are associated with a diverse group of human disorders and syndromes, collectively termed neurocristopathies, and include craniofacial abnormalities, a class of birth defects that account for nearly one-third of congenital anomalies, Hirschsprung’s disease, characterized by aganglionic megacolon, and Waardenburg’s syndrome, that includes deafness and pigment defects. This diversity is consistent with the variety of neural crest tissue derivatives that are evident. Understanding molecular pathways impingent upon and within neural crest provides insight into integral developmental signaling pathways involved in tissue induction, cellular proliferation, migration, and plasticity as well as the underlying causal factors in diseases of the neural crest. In order to place speci7c defects in perspective, this chapter will serve as an overview of neural crest–related developmental biology and genetics with some emphasis on the involvement of neural crest in cartilage and bone formation of the face and head. Several authoritative books summarize studies that have elucidated the cell biology of neural crest in the context of embryonic development (Hall and Hörstadius, 1988; Hall, 1999; Le Douarin and Kalcheim, 1999; Saint-Jeannet, 2006). Speci7c examples of gene defects associated with instructive developmental disorders will be emphasized here and in ensuing chapters.
7
Chhabra, Seema, Smrity Sahu, Keshav Sharma, Maryada Sharma, Lekha Rani, Ranjana Minz, and Sunil Dogra. "Th17/IL-17, Immunometabolism and Psoriatic Disease: A Pathological Trifecta." In Psoriasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102633.
Full textAbstract:
The burgeoning arena of immunometabolism provides evidence of how cellular, as well as local (tissue)/systemic metabolic pathways, are playing an important role in controlling immunity and inflammation. An intricate and elaborate network of various metabolic circuits specifically glycolysis, fatty acid oxidation and synthesis and amino acid metabolism precisely generate metabolites that rewire the immune response. Psoriasis is a chronic progressive self-perpetuated “IL-17-centric” inflammatory disease characterized by the co-existence of autoimmune and autoinflammatory pathways. Metabolic responses, governed by oxygen levels, nutrient availability, growth factors, cytokines, AMP/ATP ratios and amino acids, play a pivotal role in programming Th17 cell fate determination. Understanding the intricate interactions and complex interplay of molecular mechanisms responsible for Th17 cell metabolic rewiring, an important determinant of Th17 cell plasticity and heterogeneity, holds the potential to reshape psoriatic therapeutics in ways currently unimagined. This chapter entails with most recent updates on major cellular and systemic metabolic pathways regulating differentiation of Th17 cells as well their cross-talk with intracellular signaling mediators and also sheds light on how dysregulation of these pathways can be responsible for immune impairment and development of psoriatic disease. A better understanding of these metabolic processes could unveil an intriguing leverage point for therapeutic interventions to modulate metabolic programming and Th17 cell responses in this multi-systemic inflammatory disease.
8
Guido, William. "Development of Corticothalamic Projections." In The Cerebral Cortex and Thalamus, edited by Chinfei Chen, 554–62. Oxford University PressNew York, 2023. http://dx.doi.org/10.1093/med/9780197676158.003.0053.
Full textAbstract:
Abstract This chapter discusses the recent advances and current understanding of the development of corticothalamic projections. These projections arise from subpopulations of cortical neurons that reside in layers V and VI. Distinct in their pattern of thalamic innervation and function, descending projections from layers 5 and 6 also exhibit somewhat different developmental plans. The chapter focuses on their origin, cell fate, axon guidance, and layer-specific targeting of thalamic nuclei. The author also explores the impact that corticothalamic projections have on the development and plasticity of other major ascending tracts, including the thalamocortical and retinogeniculate pathways.
9
Traub, R. D., M. A. Whittington, and A. Draguhn. "Gap Junctions Between Pyramidal Cells Account for a Variety of Very Fast Network Oscillations (>80 Hz) in Cortical Structures." In Network Functions and Plasticity, 301–20. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-803471-2.00013-8.
Full text
10
"The Development of Form and Function in Fishes and the Question of Larval Adaptation." In The Development of Form and Function in Fishes and the Question of Larval Adaptation, edited by Ian A. Johnston and Thomas E. Hall. American Fisheries Society, 2004. http://dx.doi.org/10.47886/9781888569582.ch5.
Full textAbstract:
<em>Abstract.</em>—Three phases of myogenesis have been identified in the myotomal muscles of larval teleosts. The commitment of embryonic slow and fast muscle lineages is determined prior to segmentation (embryonic myogenesis) and involves notochord and floorplate derived signaling pathways, which drive the adaxial cells to a slow muscle fate. The adaxial cells elongate to span the entire somite width and subsequently migrate through the myotome to form a superficial layer of slow muscle fibers. The remaining cells of the lateral mesoderm adopt the default fast muscle phenotype. The second phase of fiber expansion in the myotomes involves recruitment from discrete germinal zones for both slow and fast muscle fibers (stratified hyperplasia). Finally, myogenic precursor cells are activated throughout the myotome (mosaic hyperplasia). The progeny of these cells either fuse to form additional fibers on the surface of existing muscle fibers or are absorbed by fibers as they expand in diameter (hypertrophic growth). There is considerable species diversity with respect to the timing of innervation of the embryonic muscle fibers in relation to other developmental events, the degree of maturation of the muscle fibers at hatching, and the onset and relative importance of stratified and mosaic hyperplasia to growth during larval life. A subset of myogenic cells specified by their position in the anterior myotomes are thought to migrate out and populate the pectoral fin buds leading to the differentiation of the pectoral fin muscles. Little is known about the mechanism of formation of the unpaired fin muscles, which occurs after the differentiation of the myotomes and is often delayed until relatively late in larval life. During ontogeny, embryonic isoforms of the myofibrillar proteins are replaced by larval and adult isoforms, and the adult multiterminal pattern of slow muscle innervation gradually develops, reflecting changes in swimming style and performance as body size increases. The body length at which particular protein isoforms are switched on varies for each myofibrillar component and with temperature. In general, early larval stages show a greater reliance on aerobic metabolic pathways and a lower capacity for anaerobic glycolysis than later larval and juvenile stages. Temperature has a marked effect on the ultrastructure, number, and phenotype of larval muscle fibers. Recent evidence suggests that egg incubation temperature can influence myogenic cell commitment, producing long-term consequences for fiber recruitment and growth performance during subsequent stages of the life cycle. The ecological significance of the phenotypic plasticity of muscle growth and some potential applications to fisheries science are briefly discussed.
Conference papers on the topic "Cell fat plasticity"
1
Crawford, Howard C. "Abstract IA-18: Epithelial cell plasticity in pancreatic cancer: The function and fate of metaplastic tuft cells." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-ia-18.
Full text
2
Scheel, C. "Abstract ES10-3: Cell fate plasticity during breast cancer development - where is the translational utility?" In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-es10-3.
Full text
3
Blanpain, C. "Abstract ES10-1: Cellular Plasticity, Fate, Potential and Lineage Commitment of Mammary Gland Stem Cells." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-es10-1.
Full text
4
Ozaltun, Hakan, and Barry H. Rabin. "Thermo-Mechanical Performance Assessment of Selected Plates From MP-1 High Power Experiments." In ASME 2017 Nuclear Forum collocated with the ASME 2017 Power Conference Joint With ICOPE-17, the ASME 2017 11th International Conference on Energy Sustainability, and the ASME 2017 15th International Conference on Fuel Cell Science, Engineering and Technology. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/nuclrf2017-3271.
Full textAbstract:
Monolithic plate-type fuel is a fuel form that is being developed for the conversion of high performance research and test reactors to low-enrichment uranium fuels. These fuel-plates are comprised of a high density, low enrichment, U-Mo alloy based fuel foil encapsulated in an aluminum cladding. To benchmark this new design, number of plates has been irradiated with satisfactory performance. As a part of continuing evaluation efforts, a set of plates covering range of operational parameters is scheduled to be tested during MP-1 irradiation experiments. It is necessary to evaluate the thermo-mechanical performance of plates during irradiation. For this, selected plates with distinct operational histories; covering low power, high power and high fission density were simulated. Fully coupled three-dimensional models of plates with a capability to evolve mechanical and thermal properties of constituent materials with irradiation time and burn-up were developed. The models input used projected parameters, including plate geometry, irradiation history and coolant conditions as input. The model output included temperature, displacement and stresses in the fuel, cladding and diffusion barrier. The fuel behavioral model considered inelastic behavior including volumetric swelling due to solid and gaseous products, irradiation induced creep, thermal expansion, conductivity degradation and plasticity. A visco-plastic behavioral model was used for the cladding that included thermal creep, irradiation hardening, growth due to fast neutrons and Mises plasticity. The plates were then simulated by using projected irradiation parameters. The resulting temperature, displacement and stress-strains were comparatively evaluated on the selected paths. The results were then compared with those of plates from previous RERTR experiments.