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Artykuły w czasopismach na temat "Heterogeneity and plasticity"
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Margadant, Coert. "Endothelial heterogeneity and plasticity". Angiogenesis 24, nr 2 (maj 2021): 197–98. http://dx.doi.org/10.1007/s10456-021-09794-6.
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Friedmann-Morvinski, Dinorah. "Glioblastoma Heterogeneity and Cancer Cell Plasticity". Critical Reviews in Oncogenesis 19, nr 5 (2014): 327–36. http://dx.doi.org/10.1615/critrevoncog.2014011777.
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Meacham, Corbin E., i Sean J. Morrison. "Tumour heterogeneity and cancer cell plasticity". Nature 501, nr 7467 (wrzesień 2013): 328–37. http://dx.doi.org/10.1038/nature12624.
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Morel, F., i N. Huyen. "Plasticity and damage heterogeneity in fatigue". Theoretical and Applied Fracture Mechanics 49, nr 1 (luty 2008): 98–127. http://dx.doi.org/10.1016/j.tafmec.2007.10.006.
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Pabst, Reinhard. "Plasticity and heterogeneity of lymphoid organs". Immunology Letters 112, nr 1 (wrzesień 2007): 1–8. http://dx.doi.org/10.1016/j.imlet.2007.06.009.
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Marjanovic, Nemanja D., Robert A. Weinberg i Christine L. Chaffer. "Cell Plasticity and Heterogeneity in Cancer". Clinical Chemistry 59, nr 1 (1.01.2013): 168–79. http://dx.doi.org/10.1373/clinchem.2012.184655.
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BACKGROUND Heterogeneity within a given cancer arises from diverse cell types recruited to the tumor and from genetic and/or epigenetic differences amongst the cancer cells themselves. These factors conspire to create a disease with various phenotypes. There are 2 established models of cancer development and progression to metastatic disease. These are the clonal evolution and cancer stem cell models. CONTENT The clonal evolution theory suggests that successive mutations accumulating in a given cell generate clonal outgrowths that thrive in response to microenvironmental selection pressures, dictating the phenotype of the tumor. The alternative cancer stem cell (CSC) model suggests that cancer cells with similar genetic BACKGROUNDs can be hierarchically organized according to their tumorigenic potential. Accordingly, CSCs reside at the apex of the hierarchy and are thought to possess the majority of a cancer's tumor-initiating and metastatic ability. A defining feature of this model is its apparent unidirectional nature, whereby CSCs undergo symmetric division to replenish the CSC pool and irreversible asymmetric division to generate daughter cells (non-CSCs) with low tumorigenic potential. However, evolving evidence supports a new model of tumorigenicity, in which considerable plasticity exists between the non-CSC and CSC compartments, such that non-CSCs can reacquire a CSC phenotype. These findings suggest that some tumors may adhere to a plastic CSC model, in which bidirectional conversions are common and essential components of tumorigenicity. SUMMARY Accumulating evidence surrounding the plasticity of cancer cells, in particular, suggests that aggressive CSCs can be created de novo within a tumor. Given the current focus on therapeutic targeting of CSCs, we discuss the implications of non-CSC-to-CSC conversions on the development of future therapies.
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Khan, Arshad, Vipul Kumar Singh, Robert L. Hunter i Chinnaswamy Jagannath. "Macrophage heterogeneity and plasticity in tuberculosis". Journal of Leukocyte Biology 106, nr 2 (2.04.2019): 275–82. http://dx.doi.org/10.1002/jlb.mr0318-095rr.
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Lüönd, Fabiana, Stefanie Tiede i Gerhard Christofori. "Breast cancer as an example of tumour heterogeneity and tumour cell plasticity during malignant progression". British Journal of Cancer 125, nr 2 (6.04.2021): 164–75. http://dx.doi.org/10.1038/s41416-021-01328-7.
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AbstractHeterogeneity within a tumour increases its ability to adapt to constantly changing constraints, but adversely affects a patient’s prognosis, therapy response and clinical outcome. Intratumoural heterogeneity results from a combination of extrinsic factors from the tumour microenvironment and intrinsic parameters from the cancer cells themselves, including their genetic, epigenetic and transcriptomic traits, their ability to proliferate, migrate and invade, and their stemness and plasticity attributes. Cell plasticity constitutes the ability of cancer cells to rapidly reprogramme their gene expression repertoire, to change their behaviour and identities, and to adapt to microenvironmental cues. These features also directly contribute to tumour heterogeneity and are critical for malignant tumour progression. In this article, we use breast cancer as an example of the origins of tumour heterogeneity (in particular, the mutational spectrum and clonal evolution of progressing tumours) and of tumour cell plasticity (in particular, that shown by tumour cells undergoing epithelial-to-mesenchymal transition), as well as considering interclonal cooperativity and cell plasticity as sources of cancer cell heterogeneity. We review current knowledge on the functional contribution of cell plasticity and tumour heterogeneity to malignant tumour progression, metastasis formation and therapy resistance.
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Sun, Wenfei, Salvatore Modica, Hua Dong i Christian Wolfrum. "Plasticity and heterogeneity of thermogenic adipose tissue". Nature Metabolism 3, nr 6 (czerwiec 2021): 751–61. http://dx.doi.org/10.1038/s42255-021-00417-4.
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Lee, Sunju, Inho Choi i Young-Kwon Hong. "Heterogeneity and Plasticity of Lymphatic Endothelial Cells". Seminars in Thrombosis and Hemostasis 36, nr 03 (kwiecień 2010): 352–61. http://dx.doi.org/10.1055/s-0030-1253457.
Pełny tekst źródłaRozprawy doktorskie na temat "Heterogeneity and plasticity"
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Chappell, Joel. "Vascular smooth muscle cell heterogeneity and plasticity in models of cardiovascular disease". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/274543.
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Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis and vascular injury. However, fundamental aspects of proliferation and the phenotypic changes within individual VSMCs, which underlie vascular disease remain unresolved. In particular, it is not known if all VSMCs proliferate and display plasticity, or whether individual cells can switch to multiple phenotypes. To assess whether proliferation and plasticity in disease is a general characteristic of VSMCs or a feature of a subset of cells, multi-colour lineage labelling is used to demonstrate that VSMCs in injury-induced neointimal lesions and in atherosclerotic plaques are oligo-clonal, derived from few expanding cells, within mice. Lineage tracing also revealed that the progeny of individual VSMCs contribute to both alpha Smooth muscle actin (aSma)-positive fibrous cap and Mac-3-expressing macrophage-like plaque core cells. Co-staining for phenotypic markers further identified a double-positive aSma+ Mac3+ cell population, which is specific to VSMC-derived plaque cells. In contrast, VSMC-derived cells generating the neointima after vascular injury generally retained expression of VSMC markers and upregulation of Mac3 was less pronounced. Monochromatic regions in atherosclerotic plaques and injury-induced neointima did not contain VSMC-derived cells expressing a different fluorescent reporter protein, suggesting that proliferation-independent VSMC migration does not make a major contribution to VSMC accumulation in vascular disease. Similarly, VSMC proliferation was examined in an Angiotensin II perfusion model of aortic aneurysm in mice, oligo-clonal proliferation was observed in remodelling regions of the vasculature, however phenotypic changes were observed in a large proportion of VSMCs, suggesting that the majority of VSMCs have some potential to modulate their phenotype. To understand the mechanisms behind the inherent VSMC heterogeneity and observed functionality, the single cell transcriptomic techniques Smart-seq2 and the Chromium 10X system were optimized for use on VSMCs. The work within this thesis suggests that extensive proliferation of a low proportion of highly plastic VSMCs results in the observed VSMC accumulation after injury, and the atherosclerotic and aortic aneurysm models of cardiovascular disease.
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Folguera, Blasco Núria. "Stochastic modelling of epigenetic regulation: analysis of its heterogeneity and its implications in cell plasticity". Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/666963.
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En aquesta tesi doctoral, el nostre objectiu principal és entendre la importància de la regulació epigenètica en la determinació del destí cel lular i de les seves possibles tran- sicions cap a altres estats. Per tal d’estudiar-ho, en primer lloc, formulem un model es- tocàstic de regulació epigenètica. En aquest model, ens centrem en l’anàlisi de la reprogra- mació cel·lular, és a dir, la situació on el sistema es mou de l’epi-fenotip diferenciat, carac- teritzat per tenir el sistema de regulació epigenètica pel gen de diferenciació(pluripotència) obert(tancat), cap a l’epi-fenotip pluripotent, definit en aquest cas per tenir el sistema de regulació epigenètica pel gen de diferenciació (pluripotència) tancat(obert).
En particular, dins de la heterogeneïtat intrínsica dels sistemes de regulació epigenètica, nosaltres identifiquem l’existència de dos possibles escenaris: l’escenari resistent, on la reprogramació no pot tenir lloc, i l’escenari plàstic, que és el qual permet el canvi de l’epi-fenotip diferenciat a l’epi-fenotip pluripotent. Aquest darrer escenari, relacionat amb l’existència de plasticitat epigenètica, ha estat associat amb envelliment. De fet, quan al model de regulació epigenètica només s’hi consideren efectes d’envelliment, el sistema representa un estat plàstic saludable, on les propietats de cèl·lula mare són adquirides de forma temporal, ja que el sistema de regulació epigenètica pot retornar a l’epi-fenotip diferenciat. Aquesta situació és la que probablement és responsable de regenerar i rejuvenir els teixits i, per tant, és la situació desitjada, ja que permetria un envelliment ‘saludable’. No obstant, quan als efectes de l’envelliment se li sumen alteracions de l’activitat epigenètica, que són freqüents a mesura que s’envelleix, l’estat plàstic esdevé un estat plàstic patològic, on en aquest cas, les propietats de cèl lula mare són adquirides de forma irreversible, és a dir, són permanents. Aquest escenari és el que probablement predisposa el sistema al càncer, ja que implica l’acumulació d’epi-fenotips indecisos que tenen el sistema de regulació epigenètica pel gen de pluripotècia obert, és a dir, que aquest gen es pot expressar.
Per tal d’estudiar aquesta situació més en detall, formulem un context general per a l’estudi d’un model estocàstic d’escales múltiples conjunt per a la regulació epigenètica i la xarxa de regulació genètica. En particular, nosaltres ens centrem en una xarxa de regulació genètica formada per 2 gens, un gen que promou la diferenciació i un gen que promou la pluripotència. Quan analitzem aquest model conjunt, veiem que el paper que juga la regulació epigènetica és cabdal ja que permet a la xarxa de regulació epigenètica canviar d’estat, en altres paraules, permet un canvi del destí cel·lular de l’epi-fenotip diferenciat a l’epi-fenotip pluripotent (reprogramació) o el canvi invers (diferenciació).
Aquest model conjunt ens permet identificar els sistemes de regulació epigenètica responsables d’atrapar la cèl·lula en un estat de cèl·lula mare, impedint-ne la seva diferenciació. La nostra formulació ens permet disenyar estratègies epigenètiques amb les quals podem aconseguir cèl·lules amb alta probabilitat de diferenciació, partint de cèl lules que inicialment eren resistents a la diferenciació. Com hom pot imaginar, aquestes estratègies són molt rellevants per a l’estudi i el tractament del càncer i altres malalties associades amb l’envelliment.In this thesis, we aim at understanding the importance of epigenetic regulation(ER) in cell fate decisions and transitions. In order to address this issue, we first formulate a stochastic model of epigenetic regulation. Within this model, we focus our discus- sion in cell reprogramming, i.e. the system moves from the differentiated epi-phenotype, characterised by differentiation(pluripotency) ER system open(closed), to the pluripotent epi-phenotype, where the ER system for differentiation(pluripotency) is closed(open). In particular, within the intrinsic heterogeneity existing in ER systems, we identify the appearance of two relevant scenarios: the resilient scenario, where reprogramming cannot occur, and the plastic one, which is the one allowing for the switch from the di erentiated epi-phenotype to the pluripotent epi-phenotype. The latter, which is characterised by ex- hibiting epigenetic plasticity, has been linked to ageing. In fact, when just ageing e ects are considered in the ER model, the system displays a `healthy' plasticity, where the stem-cell like properties can be acquired, but then, the ER system can go back to the dif- ferentiated epi-phenotype. This scenario may be related to regeneration and rejuvenation of tissues. Nevertheless, when ageing is considered along with epigenetic dis-regulations, which are likely to occur withing ageing cells/tissues, the plastic state leads to a patholog- ical plasticity, where stem cell features are acquired irreversibly. This scenario is the one which may predispose the system to cancer, as it implies the accumulation of undecided epi-phenotypes with the pluripotency ER system sustained in its on state. In order to further analyse this issue, we formulate a general framework for the study of a combined epigenetic regulation-gene regulatory network (ER-GRN)stochastic multi- scale model, which we later focus on our particular case of interest, i.e. a 2 gene regulatory network with one gene promoting differentiation and one gene promoting pluripotency. When analysing the ER-GRN model formulated, we show that the role played by ER is central since it allows the GRN to switch state, i.e. cell fate transitions from the differ- entiated phenotype to the pluripotent one (reprogramming) or vice versa (differentiation). The ER-GRN model allows to identify which ER systems are responsible for locking the cell in a stem cell like state and our formulation allows us to design epigenetic-based strategies able to obtain differentiation-primed cells from differentiation-resilient cells. Such strategies are of key relevance in the treatment of cancer and other age-associated diseases.
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DI, FILIPPO MARZIA. "NEW CONSTRAINT-BASED APPROACHES TO TACKLE THE MULTIPLE SIDES OF CELL METABOLIC PLASTICITY AND HETEROGENEITY". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241163.
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Plasticity, heterogeneity and modelling approach constitute the three pillars on the top of which this thesis investigates the complexity of cell metabolism. The multiple sides of metabolic plasticity have been explored as cell adaptive response to varying conditions, demand and perturbations under both physiological and pathological conditions. By investigating cell populations as homogeneous and heterogeneous systems, new in silico predictive models and novel computational constraint-based methodologies have been defined.
This work started from the investigation of cell populations as homogeneous systems, where the average behaviour is described and cell-to-cell differences are temporarily hidden. Reconstructing high-quality genome-scale metabolic models is crucial to computationally address cell metabolism and organize all the available metabolic knowledge of given cells or organisms. Although multiple tools for performing this task already exist, a pipeline for the semi-automatic reconstruction of genome-scale networks has been proposed to solve some current critical issues and generate higher quality models. The application of this approach for the genome-wide metabolic reconstruction of yeast Zygosaccharomyces parabailii showed adherence of in silico simulations to experimental data and literature findings. Moreover, metabolic plasticity in response to different metabolic regimes has been explored through constraint-based modelling.
The potentialities of genome-scale reconstructions in mirroring the systemic perspective coexist with difficulty in their management. In this work, greater control is achieved by switching to smaller-scale core networks. In particular, core modelling has been exploited as an effective mean to investigate intertumoural heterogeneity, and plasticity of the implemented tumour metabolic programs as adaptation to different environmental scenarios.
The effectiveness of homogeneous systems to lower overall system complexity level without compromising biological validity of in silico outcomes goes along with the need to address cell-to-cell variations of cell populations. In this regard, classic constraint-based modelling has been extended to deal with heterogeneous systems. A new strategy, called popFBA, has been developed to reconstruct and simulate cell populations metabolism, by putting emphasis on the relationships established among their components. Using as case study the ecosystemic view of cancer populations, popFBA highlighted that the achievement of optimal biomass is consistent with metabolic plasticity of population components under different scenarios together with a cooperative behaviour. At the same time, countless combinations of flux distributions for the individual population components prompted to develop a novel methodology called single-cell Flux Balance Analysis (scFBA). This metodology integrates single-cell transcriptomics data as further constraints on the individual components through the computation for each reaction of a Reaction Activity Score, which we implemented in a previous computational framework called MaREA. In this way, scFBA efficiently reduced the amount of allowable individual flux distributions, and captured complex networks of interactions between cells of a specific population.
In view of the findings of this research, a deep characterization of metabolic plasticity within cell populations and of the intricate dialogue between cells and their environment can assist the formulation of more rational and personalized strategies. Their devising could enable to hamper disease progression, or to exploit metabolism of given microorganisms for producing relevant chemical compounds.Plasticity, heterogeneity and modelling approach constitute the three pillars on the top of which this thesis investigates the complexity of cell metabolism. The multiple sides of metabolic plasticity have been explored as cell adaptive response to varying conditions, demand and perturbations under both physiological and pathological conditions. By investigating cell populations as homogeneous and heterogeneous systems, new in silico predictive models and novel computational constraint-based methodologies have been defined. This work started from the investigation of cell populations as homogeneous systems, where the average behaviour is described and cell-to-cell differences are temporarily hidden. Reconstructing high-quality genome-scale metabolic models is crucial to computationally address cell metabolism and organize all the available metabolic knowledge of given cells or organisms. Although multiple tools for performing this task already exist, a pipeline for the semi-automatic reconstruction of genome-scale networks has been proposed to solve some current critical issues and generate higher quality models. The application of this approach for the genome-wide metabolic reconstruction of yeast Zygosaccharomyces parabailii showed adherence of in silico simulations to experimental data and literature findings. Moreover, metabolic plasticity in response to different metabolic regimes has been explored through constraint-based modelling. The potentialities of genome-scale reconstructions in mirroring the systemic perspective coexist with difficulty in their management. In this work, greater control is achieved by switching to smaller-scale core networks. In particular, core modelling has been exploited as an effective mean to investigate intertumoural heterogeneity, and plasticity of the implemented tumour metabolic programs as adaptation to different environmental scenarios. The effectiveness of homogeneous systems to lower overall system complexity level without compromising biological validity of in silico outcomes goes along with the need to address cell-to-cell variations of cell populations. In this regard, classic constraint-based modelling has been extended to deal with heterogeneous systems. A new strategy, called popFBA, has been developed to reconstruct and simulate cell populations metabolism, by putting emphasis on the relationships established among their components. Using as case study the ecosystemic view of cancer populations, popFBA highlighted that the achievement of optimal biomass is consistent with metabolic plasticity of population components under different scenarios together with a cooperative behaviour. At the same time, countless combinations of flux distributions for the individual population components prompted to develop a novel methodology called single-cell Flux Balance Analysis (scFBA). This metodology integrates single-cell transcriptomics data as further constraints on the individual components through the computation for each reaction of a Reaction Activity Score, which we implemented in a previous computational framework called MaREA. In this way, scFBA efficiently reduced the amount of allowable individual flux distributions, and captured complex networks of interactions between cells of a specific population. In view of the findings of this research, a deep characterization of metabolic plasticity within cell populations and of the intricate dialogue between cells and their environment can assist the formulation of more rational and personalized strategies. Their devising could enable to hamper disease progression, or to exploit metabolism of given microorganisms for producing relevant chemical compounds.
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Konnully, Augustus Meera Bessy. "Characterization of cellular heterogeneity in Diffuse Low Grade Glioma". Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT038.
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Les gliomes diffus de bas grade (DLGG) sont des tumeurs gliales de grade II qui affectent principalement les jeunes adultes. Elles sont caractérisées par une croissance lente et une activité mitotique réduite. Cependant, ces tumeurs diffusent et envahissent le cerveau sain via les vaisseaux sanguins et les fibres nerveuses. Après plusieurs années de croissance lente, ces tumeurs peuvent évoluer vers des glioblastomes, des tumeurs cérébrales très agressives dont la survie médiane moyenne est alors de 12 à 15 mois après le diagnostic. La caractérisation cellulaire des DLGG est encore limitée ce qui nuit à la recherche d’un traitement à un stade précoce. Dans ma thèse de doctorat, je me suis focalisée sur la caractérisation de 'hétérogénéité cellulaire des DLGG mutés pour IDH1. En effectuant une analyse d'immunofluorescence sur des astrocytomes et oligodendrogliomes de grade II, j'ai identifié deux sous-populations cellulaires largement non chevauchantes et exprimant respectivement les facteurs de transcription SOX9 et OLIG1. Ces cellules s’apparentent à des cellules de type astrocytaire et oligodendrocytaire et expriment des marqueurs moléculaires distincts. Les cellules SOX9 expriment APOE, KCNN3, CRYAB et ID4, tandis que les cellules OLIG1 expriment préfentiellement PDGFRA, SOX8, MASH1 et SOX4. Par ailleurs, j’ai montré que les cellules SOX9 présentent une activation particulière des voies de signalisation, notamment Notch, BMP et leurs cibles en aval. Pour étudier le rôle de la voie de signalisation Notch dans la formation de ces 2 sous-populations tumorales, j'ai purifié par tri magnétique les cellules tumorales à partir d'échantillons de gliomes fraîchement réséqués et j'ai surexprimé le domaine intracellulaire Notch (NICD), une forme active de Notch. J’ai ainsi montré que cette activation augmentait l’expression des marqueurs cellulaires associés aux cellules SOX9+ et une baisse de ceux associés aux cellules OLIG1+. J'ai ensuite étendu ces analyses à une lignée cellulaire anaplasique dérivée d'un patient et mutée pour IDH1. Ces résultats indiquent un rôle clé de la signalisation Notch dans la régulation de la plasticité des cellules tumorales. Des expériences similaires pour étudier l'activation de la signalisation BMP (bone morphogenetic protein) n'ont pas montré d'effet notable sur la plasticité. Néanmoins, le traitement des cellules par des membres de la famille BMP a fortement augmenté l’expression de CRYAB, un marqueur associé à SOX9, et a diminué l’expression de OLIG1 et OLIG2. En conclusion, j'ai identifié deux sous-populations tumorales non chevauchantes dans des gliomes diffus de bas grade et j'ai démontré le rôle déterminant de la voie de signalisation Notch dans leur formation. Ces résultats permettront de mieux comprendre l'hétérogénéité tumorale dans les DLGG et de concevoir de nouvelles stratégies thérapeutiques contre ces tumeursDiffuse Low-Grade Gliomas (DLGG) are WHO grade II glial tumors affecting younger adults. They are characterized as silent, slow growing tumors with fewer mitotic activities. However, they diffuse and invade the healthy brain via blood vessels and nerve fibers. These, over a period of years develop to malignant Glioblastoma, aggressive brain tumors where patients have an average medial survival of 12-15 months after diagnosis. Ill-defined phenotypic and cellular diversity of DLGG poses serious limitation to treatment and prevention at the early stage.In my PhD thesis, I aimed to address this limitation by characterizing the cellular heterogeneity in IDH1-mutated DLGG. By performing immunofluorescence analysis on grade II astrocytoma and oligodendroglioma, I have identified two largely non-overlapping cellular subpopulations expressing SOX9 and OLIG1 transcription factors, which represent astrocyte-like and oligodendrocyte-like cells, respectively. Upon further investigation, I have shown that these subpopulations express distinct molecular markers. Sox9 cells are associated with APOE, KCNN3, CRYAB and ID4, while Olig1 cells showed strong correlation with the expression of PDGFRA, SOX8, MASH1, and SOX4. In addition, the sox9 cells show a particular activation of signaling pathways including Notch, BMP and their downstream targets.To ascertain the role of Notch signaling in regulating the formation of these tumoral subpopulations, I used magnetic sorting of tumor cells from freshly resected glioma samples and overexpressed Notch Intracellular Domain (NICD), an active form of Notch. Increased Notch activation resulted in an upregulation of Sox9- and downregulation of Olig1-associated cell markers. I have then extended these analyses on one anaplastic IDH1 mutated patient derived cell line which reproduced similar gene expression profile confirming the robustness of the role of Notch signaling in regulating the plasticity of the cells. Parallel experiments performed by activation of Bone Morphogenetic Protein (BMP) signaling on IDH1 mutated cell line did not show a prominent effect on the plasticity. Nevertheless, BMP signal activation highly upregulated CRYAB, a SOX9 related marker and downregulated OLIG1 and OLIG2.In conclusion, I have identified two non-overlapping tumor subpopulations in diffuse low-grade gliomas and demonstrated the deterministic role of Notch signaling pathway in their formation. I believe that these findings would aid in better understanding tumoral heterogeneity in DLGG and be extended in designing new therapeutic strategies against these tumors
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du, Plessis Darren Scott. "Temporal interactions with flamingo foraging plasticity: ecological effects on basal resources and benthic heterogeneity". Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29623.
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The role of predation as a structuring agent of communities has been a focal area of research in marine ecology. Conversely, studies focusing on foraging plasticity, particularly by shorebirds, and consequences for benthic community structure, heterogeneity and ecosystem functioning have been limited in marine soft-sediments. Temporal interactions with foraging plasticity is an even greater knowledge gap. The primary goal of this dissertation was to expand on current understanding of foraging plasticity and the broader ecological role of Greater Flamingos as predators in marine sedimentary ecosystems. The specific aim was to test the long-term effects of different foraging structure sizes (which is a subtle form of foraging plasticity) on sedimentary assemblages following foraging disturbances. In situ comparisons of large and small foraging structures created by the flamingos with adjacent non-foraged sediments (controls) indicated that small channels had greater concentrations of sediment organic matter relative to large channels following feeding. Additionally, small feeding structures supported greater abundances of the burrowing amphipod Urothoe grimaldii and the grazing gastropod Assiminea globulus along with elevated size-specific sediment deposition rates. These results shed light on the differential timedependent impacts flamingo foraging plasticity can generate on basal trophic resources and higher consumers. Results also showed that irrespective of size, feeding channels made by flamingos generally became enriched with microalgae following foraging, with this enrichment effects spilling over into non-foraged controls sediments. This indicates that foraging by flamingos has the potential to create resource islands that become enriched with microalgae over time, with effects spilling over into adjacent non-foraged areas. Importantly, these positive effects may oppose the negative effects of bioturbation by burrowing sandprawns on productivity, which is a dominant process in the study area. This study emphasizes the importance of Greater Flamingos in regulating basal resource supply, community structure and spatio-temporal heterogeneity and has highlighted the need for predation models within sedimentary environments to incorporate time-dependent effects of foraging plasticity into current thinking.
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Chi, Ma. "Improving the Plasticity of Metallic Glass through Heterogeneity Induced by Electropulsing-assisted Surface Severe Plastic Deformation". University of Akron / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=akron1555595868348676.
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Einsmann, Juliet Caroline Jr. "Nutrient Foraging in Ten Southeast Coastal Plain Plant Species". Thesis, Virginia Tech, 1998. http://hdl.handle.net/10919/36849.
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Plant root system response to nutrient heterogeneity was tested in ten plant species of varying life form and successional status. All plants tested are native to the South Carolina coastal plain. Morphological responses of the root system (scale, precision and discrimination) and overall plant response (sensitivity) to increasing nutrient heterogeneity were tested. Ten individuals of each species were placed into four treatments which had varying nutrient distribution but the same overall nutrient addition. Plants were harvested when roots reached pot edge. I observed high variation in scale (mass and extent of a root system), precision (the ability to proliferate roots in nutrient patches) and sensitivity (growth benefits gained as nutrient heterogeneity increases; measured as total biomass). No significant discrimination responses were observed, although greatest mean root density occurred at intermediate fertility levels for all species. I tested the hypothesis that scale and precision would be negatively correlated, and I did not observe this relationship in these plant species. However, in herbaceous species scale and precision were positively correlated. Sensitivity was not closely related to precision indicating that proliferating roots in fertile patches does not always yield growth benefits in heterogeneous soils. Further, some sensitive species had very low precision suggesting that other characteristics lead to positive growth response in heterogeneous environments. Plasticity of root uptake rates and demography of roots are proposed as two other mechanisms which may play important roles in plant sensitivity responses. Scale was negatively correlated to sensitivity for herbaceous plants suggesting that plants that monopolize the most soil space are not able to gain benefits from nutrient patches within the soil matrix. There was no trend observed to suggest that plant life form was correlated with precision or sensitivity. However, scale was greater in herbs than in woody plants, possibly because the two life forms develop at different times.Master of Science
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Conlon, Kelly Timothy. "The effect of mesoscopic spatial heterogeneity on the plastic deformation of Al-Cu alloys". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0004/NQ42838.pdf.
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Li, Xiaoshuang. "Identification and Phenotypic Plasticity of Metastatic Cells in a Mouse Model of Melanoma". FIU Digital Commons, 2017. http://digitalcommons.fiu.edu/etd/3472.
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Melanoma is the deadliest form of skin cancer due to its high propensity to metastasize and resistance to current therapies. We have created a spontaneous mouse model of metastatic melanoma (Dct-Grm1/K5-Edn3) where metastasis to the lungs is 80% penetrant. The primary tumors of these mice present cellular heterogeneity with cells at varying levels of differentiation. The main goal of this study was to determine the metastatic potential of the primary tumor resident Tyrosinase positive cells and evaluate the dynamic phenotypic changes as those cells move from the primary tumors to the sites of metastasis. To accomplish this aim I crossed the Dct-Grm1/K5-Edn3 mice to CreERT2/mT/mG mice to indelibly label Tyrosinase cell populations within the primary tumor with Green Fluorescent Protein (GFP) by topical application of 4-hydroxytamoxifen (4HT) at the tumor site. In vivo lineage tracing and characterization of GFP+ cells were performed in the metastatic lesions.
In the 4HT treated Dct-Grm1/ K5-Edn3/Tyr-CreERT2/mT/mG mice, primary tumor derived Tyrosinase positive cells or their progeny (GFP+) established successful metastases in the distant organs indicating the tumorigenic capacity of the differentiated cell populations. Numerous metastatic melanoma cells were identified in the vasculature of the metastatic organs and established close association with the vascular endothelium. The intravascular cells lost pigmentation and did not express melanocytic markers; however, they mimicked endothelial cell properties and gained the expression of CD31 (also known as platelet endothelial cell adhesion molecule PECAM-1) and vascular endothelial (VE)-Cadherin. In the lung metastatic foci, GFP+ cells resumed pigmentation production and lost the expression of endothelial cell markers. Evidence from other metastatic organs in the mice further supported the phenotypic plasticity of metastatic melanoma cells.
The in vivo lineage tracing system established in the melanoma mouse model revealed tumor phenotypic plasticity and will be a powerful model to evaluate and help us understand the etiology and pathogenesis of melanoma metastasis. Further characterization of those more aggressive cells in melanoma will allow for the development of new prognostic tests and novel therapeutic strategies to eliminate metastasis.
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Madrid, Canales Ignacio. "Model of Cellular Growth under Stress : Emergence of Heterogeneity and Impact of the Environment". Electronic Thesis or Diss., Institut polytechnique de Paris, 2024. http://www.theses.fr/2024IPPAX008.
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Cette thèse porte sur l'analyse statistique et mathématique de la croissance cellulaire à l'échelle individuelle sous l'effet d'un stress. À partir de l'analyse des données recueillies par Sebastián Jaramillo et James Broughton sous la direction de Meriem El Karoui, nous avons construit différents modèles permettant une compréhension à différents niveaux de l'impact que la réponse hétérogène au stress génotoxique (réponse SOS) a sur la croissance d'une population de bactéries Escherichia coli. Pour modéliser la dynamique de ces populations on utilise des processus stochastiques à valeurs mesures.Nous construisons tout d'abord on construit un modèle stochastique basé sur le modèle "adder" de contrôle de la taille, étendu pour incorporer la dynamique de la réponse SOS et son effet sur la division cellulaire. Le cadre choisi est paramétrique et le modèle est ajusté par maximum de vraisemblance aux données de lignées individuelles obtenues en mother machine. Cela nous permet de comparer quantitativement les paramètres inférés dans différents environnements.Nous nous intéressons ensuite aux propriétés ergodiques d'un modèle plus général que "adder", répondant à des questions ouvertes sur son comportement en temps long. On considère un flot déterministe général et un noyau de fragmentation non nécessairement auto-similaire. Nous montrons l'existence des éléments propres. Ensuite, une dollar_h_dollar-transformée de Doob avec la fonction propre nous ramène à l'étude d'un processus conservatif. Enfin, en montrant une propriété de petite set pour les compacts de l'espace d'états, nous obtenons alors la convergence exponentielle du modèle.Finalement, nous considérons un modèle bitype structuré en âge modélisant la plasticité phénotypique observée dans la réponse au stress. Nous étudions la probabilité de survie et le taux de croissance de la population en environnement constant et périodique. Nous mettons en lumière un trade-off pour avoir la survie de la population, ainsi qu'une sensibilité par rapport aux paramètres du modèle qui n'est pas la même pour la probabilité de survie et pour le taux de croissance.Nous concluons avec une section indépendante, initiée durant le CEMRACS 2022. Nous étudions numériquement la propagation spatiale des populations structurés en taille modélisant le mouvement collectif de clusters de Myxobactéries à travers de systèmes d'équations de réaction-diffusionThis thesis focuses on understanding individual-scale cell growth under stress. Starting from the analysis of the data collected by Sebastián Jaramillo and James Broughton under the supervision of Meriem El Karoui, we have developed various models to comprehend the impact of the heterogeneous response to genotoxic stress (SOS response) on the growth of a Escherichia coli populations. We employ measure-values stochastic processes to model the dynamics of these populations.Firstly, we construct a stochastic model based on the "adder" size-control model, extended to incorporate the dynamics of the SOS response and its effect on cell division. The chosen framework is parametric, and the model is fitted by maximum likelihood to individual lineage data obtained in mother machine. This allows us to quantitatively compare inferred parameters in different environments.Next, we explore the ergodic properties of a more general model than the "adder," addressing open questions about its long-time behaviour. We consider a general deterministic flow and a fragmentation kernel that is not necessarily self-similar. We demonstrate the existence of eigenelements. Then, a Doob dollar_h_dollar-transform with the found eigenfunction reduces the problem to the study of a conservative process. Finally, by proving a "petite set" property for the compact sets of the state space, we obtain the exponential convergence.Finally, we consider a bitype age-structured model capturing the phenotypic plasticity observed in the stress response. We study the survival probability of the population and the population growth rate in constant and periodic environments. We evince a trade-off for population establishment, as well as a sensitivity with respect to the model parameters that differs for survival probability and growth rate.We conclude with an independent section, collaborative work initiated during CEMRACS 2022. We investigate numerically the spatial propagation of size-structured populations modeling the collective movement of Myxobacteria clusters via a system of reaction-diffusion equations
Części książek na temat "Heterogeneity and plasticity"
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Sousa, Bárbara, Ana Sofia Ribeiro i Joana Paredes. "Heterogeneity and Plasticity of Breast Cancer Stem Cells". W Stem Cells Heterogeneity in Cancer, 83–103. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_5.
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Brasier, Allan R. "Innate Immunity, Epithelial Plasticity, and Remodeling in Asthma". W Precision Approaches to Heterogeneity in Asthma, 265–85. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-32259-4_13.
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Tripathi, Shubham, Jianhua Xing, Herbert Levine i Mohit Kumar Jolly. "Mathematical Modeling of Plasticity and Heterogeneity in EMT". W Methods in Molecular Biology, 385–413. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0779-4_28.
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Soumelis, Vassili, Yong-Jun Liu i Michel Gilliet. "Dendritic Cell Biology: Subset Heterogeneity and Functional Plasticity". W The Biology of Dendritic Cells and HIV Infection, 3–43. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-33785-2_1.
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Kudo, Yoshihisa, Etsuro Ito i Akihiko Ogura. "Topographical Heterogeneity of Glutamate Agonist-Induced Calcium Increase in Hippocampus". W Excitatory Amino Acids and Neuronal Plasticity, 125–33. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_15.
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van Diggelen, Fuda, Matteo de Carlo, Nicolas Cambier, Eliseo Ferrante i Guszti Eiben. "Emergence of Specialised Collective Behaviors in Evolving Heterogeneous Swarms". W Lecture Notes in Computer Science, 53–69. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-70068-2_4.
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AbstractNatural groups of animals, such as swarms of social insects, exhibit astonishing degrees of task specialization, useful for solving complex tasks and for survival. This is supported by phenotypic plasticity: individuals sharing the same genotype that is expressed differently for different classes of individuals, each specializing in one task. In this work, we evolve a swarm of simulated robots with phenotypic plasticity to study the emergence of specialized collective behavior during an emergent perception task. Phenotypic plasticity is realized in the form of heterogeneity of behavior by dividing the genotype into two components, with a different neural network controller associated to each component. The whole genotype, which expresses the behavior of the whole group through the two components, is subject to evolution with a single fitness function. We analyze the obtained behaviors and use the insights provided by these results to design an online regulatory mechanism. Our experiments show four main findings: 1) Heterogeneity improves both robustness and scalability; 2) The sub-groups evolve distinct emergent behaviors. 3) The effectiveness of the whole swarm depends on the interaction between the two sub-groups, leading to a more robust performance than with singular sub-group behavior. 4) The online regulatory mechanism improves overall performance and scalability.
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Koyama, Motomichi, Hiroshi Noguchi i Kaneaki Tsuzaki. "Microstructural Crack Tip Plasticity Controlling Small Fatigue Crack Growth". W The Plaston Concept, 213–34. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-7715-1_10.
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AbstractIn this chapter, we present a metallurgical–mechanical mechanism-based strategy for the design of fatigue-resistant metals. Specifically, we elucidate the importance of the metallurgical microstructure in a mechanical singular field (crack tip). The fatigue crack growth resistance is controlled through the crack tip “plasticity”, and the effect of the associated microstructure becomes significant when the crack is “small (or short)”. More importantly, the resistance to small crack growth determines a major portion of fatigue life and strength. Therefore, the microstructural crack tip plasticity is a key breakthrough to the development of fatigue-resistant metals. As successful examples of this concept, we introduce the effects of grain refinement, martensitic transformation, strain aging, dislocation planarity enhancement, and microstructure heterogeneity on small fatigue crack growths.
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Kneppers, Jeroen, Andries M. Bergman i Wilbert Zwart. "Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications". W Advances in Experimental Medicine and Biology, 255–75. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11836-4_15.
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Mazloom, Amin R., Kalyan Basu, Subhrangsu S. Mandal i Sajal K. Das. "Modeling a Complex Biological Network with Temporal Heterogeneity: Cardiac Myocyte Plasticity as a Case Study". W Lecture Notes of the Institute for Computer Sciences, Social Informatics and Telecommunications Engineering, 467–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02466-5_46.
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Dewitt, Thomas J., i R. Brian Langerhans. "Integrated Solutions to Environmental Heterogeneity: Theory of Multimoment Reaction Norms". W Phenotypic Plasticity, 98–111. Oxford University PressNew York, NY, 2004. http://dx.doi.org/10.1093/oso/9780195138962.003.0007.
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Abstract Environmental change drives evolution. If environments were constant, evolution rapidly would proceed to a rather humdrum, mostly static, equilibrium. The diversity of life we see today is the result of moderate but continual environmental challenges. Put simply, the seed of creation is the strife of organisms at odds with their changing environments. The premise of this book is that environmental variation is responsible for a spectacular suite of adaptations more intricate and labile than those for dealing with fixed environments. Phenotypic plasticity is one of those adaptations, but several others exist. Among the many adaptations organisms have to cope with environmental variability are dormancy (i.e., seed banking or diapausing), to outlast problem environments; plasticity to produce relatively fit phenotypes for the demands of alternative environments; intermediate phenotypes (generalization) and bet-hedging, both of which reduce variance in performance across environments; and dispersal, to leave when environments are unfavorable. Much theoretical literature addresses the merits of each strategy, generally, compared with ecological specialization (e.g., Levins 1968; Lewontin and Cohen 1969; Cohen 1976; Lively 1986a; Seger and Brockmann 1987; Van Tienderen 1997; reviewed in Wilson and Yoshimura 1994; chapter 6).
Streszczenia konferencji na temat "Heterogeneity and plasticity"
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Durand, Simon, Valentina Boeva, Caroline Louis-Brennetot, Agathe Peltier, Cécile Pierre-Eugène, Sylvain Baulande, Olivier Delattre i Isabelle Janoueix-Lerosey. "Abstract B20: Deciphering heterogeneity and plasticity in neuroblastoma". W Abstracts: AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; December 3-6, 2017; Atlanta, Georgia. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.pedca17-b20.
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Mejias, J. F., H. J. Kappen, A. Longtin i J. J. Torres. "Short-term synaptic plasticity and heterogeneity in neural systems". W PHYSICS, COMPUTATION, AND THE MIND - ADVANCES AND CHALLENGES AT INTERFACES: Proceedings of the 12th Granada Seminar on Computational and Statistical Physics. AIP, 2013. http://dx.doi.org/10.1063/1.4776513.
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Frost, Miroslav, Petr Sedlák, Hanuš Seiner, Jan Valdman, Alexej Moskovka i Petr Šittner. "Constitutive Model for NiTi Polycrystalline Alloys Undergoing Transformation and Plastic Deformation Processes". W SMST 2024. ASM International, 2024. http://dx.doi.org/10.31399/asm.cp.smst2024p0082.
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Abstract Great attention has been recently paid to the investigation of plastic deformation in NiTi. Experimental investigations of the mechanical response of NiTi polycrystalline samples within a broad stress-strain-temperature state space have revealed a complex response involving martensitic transformation, reorientation, and plastic deformation processes. The interactions between them result in complex coupled phenomena, such as transformation-induced plasticity, martensite stabilization through plastic deformation, and micro-strain heterogeneity induced by plasticity. Plastic deformation in NiTi not only generates irrecoverable strain at the macroscale, but it also induces substantial strain heterogeneity in the microstructure. This heterogeneity significantly affects the functional properties and may open up new technology pathways for designing sophisticated products. Tailored constitutive models that can reproduce the response in complex loading scenarios can be extremely beneficial.
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Natsuizaka, Mitsuteru, Shinya Ohashi, Seiji Naganuma, Ross A. Kalman, Asami Ohyama, Ben Rhoades, Maria E. Vega i in. "Abstract 5194: Notch regulates squamous differentiation, cell plasticity and tumor heterogeneity in esophageal carcinoma". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5194.
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Ting, David T. "Abstract IA-02: Pancreatic cancer heterogeneity and plasticity: The mix of seed and soil". W 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-02.
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HANON, Guillaume. "Heterogeneity of strain and texture inside roll-bonded multilaminates". W Material Forming. Materials Research Forum LLC, 2024. http://dx.doi.org/10.21741/9781644903131-191.
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Abstract. This study demonstrates the usefulness of crystal plasticity modeling and crystallographic texture analysis when aiming to understand through-thickness strain heterogeneity after roll bonding of dissimilar materials. FE modeling was used at two length scales to study the deformation and texture heterogeneities inside a 9-layer multilaminate made of aluminum and steel, produced by roll-bonding. Microstructure and crystallographic texture were probed using EBSD. Numerical predictions indicated that plane strain compression was accompanied by significant shear parallel to the rolling plane and inclined shear banding in aluminum. Predictions of the Texture development were more accurate in the bcc phase than the fcc phase.
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Winter, Peter S., Srivatsan Raghavan, Andrew Navia, Hannah Williams, Alan DenAdel, Radha Kalekar, Jennyfer Galvez-Reyes i in. "Abstract PR03: Subtype-specific microenvironmental crosstalk and tumor cell plasticity in metastatic pancreatic cancer". W Abstracts: AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-pr03.
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Zhang, Zeda, Chuanli Zhou, Xiaoling Li, Spencer Barnes, Su Deng, Elizabeth Hoover, Chi-Chao Chen i in. "Abstract NG06: CHD1-loss confers AR targeted therapy resistance via promoting cancer heterogeneity and lineage plasticity". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-ng06.
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Clairambault, Jean. "Mathematical Modelling of Cancer Growth and Drug Treatments: Taking Into Account Cell Population Heterogeneity and Plasticity". W 2023 European Control Conference (ECC). IEEE, 2023. http://dx.doi.org/10.23919/ecc57647.2023.10178266.
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Sedlak, Petr, Miroslav Frost, Hanus Seiner, Ludek Heller i Petr Sittner. "Thermodynamical Model of NiTi SMA Including Plastic Deformation Mechanisms". W SMST2022. ASM International, 2022. http://dx.doi.org/10.31399/asm.cp.smst2022p0065.
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Abstract This paper presents an extension of a well-established constitutive model for NiTi covering both reversible (elastic, martensitic transformation, martensite reorientation) and irreversible (plastic) deformation mechanisms. Besides the inclusion of mechanisms of plastic deformation in both austenitic and martensitic phases in an independent manner, the model also newly captures more complex coupled phenomena of martensitic transformation and plastic deformation, such as transformation-induced plasticity, stabilization of martensite by plastic deformation, or plasticity-induced microstrain heterogeneity leading to functional fatigue. Despite a large number of different mechanisms involved in the model, which is reflected by a considerable number of internal parameters introduced for the description of the evolving microstructure of the material, the model still brings a basic, simple phenomenological understanding of the coupled transformation-plasticity proceeding in NiTi. After successful implementation to FEM software, the model provides new possibilities for simulations of NiTi components' behavior and processing.