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Bibliografias temáticas / Cell division and cell death

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Literatura científica selecionada sobre o tema "Cell division and cell death"

Autor: Grafiati

Publicado: 31 de agosto de 2024

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Artigos de revistas sobre o assunto "Cell division and cell death"

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Maddox, Amy Shaub, e Jan M. Skotheim. "Cell cycle, cell division, cell death". Molecular Biology of the Cell 30, n.º 6 (15 de março de 2019): 732. http://dx.doi.org/10.1091/mbc.e18-12-0819.

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Coller, Hilary A., e Arshad Desai. "Cell cycle, cell division, and cell death". Molecular Biology of the Cell 28, n.º 6 (15 de março de 2017): 693–94. http://dx.doi.org/10.1091/mbc.e16-11-0793.

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Lewis, Mark. "Cell differentiation; Cell division, growth and death". Current Opinion in Cell Biology 14, n.º 6 (dezembro de 2002): 671–72. http://dx.doi.org/10.1016/s0955-0674(02)00396-4.

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Yuan, Junying, e David Morgan. "Cell division, growth and death". Current Opinion in Cell Biology 14, n.º 6 (dezembro de 2002): 673–75. http://dx.doi.org/10.1016/s0955-0674(02)00397-6.

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Kornbluth, Sally, e Jonathon Pines. "Cell division, growth and death". Current Opinion in Cell Biology 15, n.º 6 (dezembro de 2003): 645–47. http://dx.doi.org/10.1016/j.ceb.2003.10.017.

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Reed, Steven I., e Joel H. Rothman. "Cell division, growth and death". Current Opinion in Cell Biology 16, n.º 6 (dezembro de 2004): 599–601. http://dx.doi.org/10.1016/j.ceb.2004.10.002.

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Kaufmann, Scott, e Mike Tyers. "Cell division, growth and death". Current Opinion in Cell Biology 17, n.º 6 (dezembro de 2005): 565–67. http://dx.doi.org/10.1016/j.ceb.2005.10.006.

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Earnshaw, William C., e Yuri A. Lazebnik. "Cell division, growth and death". Current Opinion in Cell Biology 18, n.º 6 (dezembro de 2006): 587–88. http://dx.doi.org/10.1016/j.ceb.2006.10.010.

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Jackson, Peter K., e Jan-Michael Peters. "Cell division, growth and death". Current Opinion in Cell Biology 19, n.º 6 (dezembro de 2007): 646–48. http://dx.doi.org/10.1016/j.ceb.2007.11.001.

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Barral, Yves, e Jürgen Knoblich. "Cell division, growth and death". Current Opinion in Cell Biology 20, n.º 6 (dezembro de 2008): 647–49. http://dx.doi.org/10.1016/j.ceb.2008.10.007.

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Teses / dissertações sobre o assunto "Cell division and cell death"

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Cheng, Jade. "Regulation of cell division and cell death by GRASP65". Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544414.

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Otake, Andreia Hanada. ""Papel de dissialogangliosídios na proliferação e morte celular induzida de melanócitos e melanomas in vitro"". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26052006-113740/.

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Dissialogangliosídios, como GD3 e derivados são marcadores da progressão de melanomas. Para avaliar as possíveis funções desta molécula, transfectamos células de melanócitos com o gene da enzima ST8Sia I, que converte GM3 em GD3. Mostramos que GD3 não interfere na capacidade proliferativa dessas células, porém a expressão de GD3 mostrou-se associada à sobrevivência celular. Melanomas adquirem autonomia quanto às vias dependentes do fator de crescimento de fibroblastos (FGF-1 e -2). A expressão de GD3 não interfere na resposta proliferativa a estes fatores, porém GD3 e outros glicoesfingolipídios de membrana modulam a resposta migratória induzida por FGF-2. A expressão de GD3 sensibiliza as células à morte celular induzida por diferentes quimioterápicos, como cisplatina e vimblastina; porém, torna as células resistentes ao tratamento com temozolamida. A sensibilização ao tratamento com vimblastina, mas não às outras drogas, depende da presença de GD3, como observado por ensaios de depleção metabólica
Disialoganglioside GD3 and its derivatives are melanoma progression markers. To evaluate the possible roles of these molecules along melanoma progression, we have transfected the GD3 synthase gene (ST8Sia I) in a melanocyte cell line. Accumulation of GD3 did not confer any proliferative advantage to melanocytes. However, GD3 expression was associated with cell survival. The autonomic growth of melanomas is in part related to a constitutive activation of fibroblast growth factor dependent pathways. GD3 expression did not alter the proliferative response to either FGF-1 or FGF-2. However, GD3 and other membrane glycospingolipids modulate the motogenic activity of FGF-2. GD3 expression sensitizes melanocytes to chemotherapeutic agent-induced cell death, as cisplatin and vimblastin. On the other hand, GD3 turned melanocytes more resistant to temozolomide. Chemosensitization to vimblastin, but not to the other drugs, was dependent on the presence of GD3 within the cells, as shown by metabolic depletion of glycosphingolipids

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Chalabi, Asma. "Processus d'analyse dynamique pour l'imagerie de cellules vivantes permettant la détection des réponses cellulaires aux anticancéreux, par traitement de l'image et du signal et apprentissage automatique profond". Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6004.

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La division et la mort cellulaires sont les principaux indicateurs permettant d'évaluer l'action des thérapies ciblées dans le cancer, et seules leurs mesures précises peuvent révéler l'efficacité réelles d'un traitement. La détection des événements de division et de mort cellulaires dans les essais sur cellules vivantes a le potentiel de produire des mesures robustes de la pharmacodynamique des anticancéreux et de permettre une compréhension plus complète des réponses de cellules tumorales aux combinaisons thérapeutiques. Connaître précisément le moment de la mort ou de la division cellulaire dans une expérience sur cellules vivantes permet d'étudier la contribution relative des différents effets des médicaments, tels que les effets cytotoxiques ou cytostatiques, sur une population de cellules. Cependant, les méthodes classiques nécessitent des colorants pour mesurer la viabilité cellulaire avec des comptages de populations à un temps final, où les taux de prolifération ne peuvent être estimés que lorsque les cellules viables et mortes sont marquées simultanément.L'imagerie de cellules vivantes est une technique prometteuse pour déterminer l'efficacité des médicaments, la principale limitation étant la précision et la profondeur des analyses pour extraire automatiquement des mesures de description de phénotypes de réponse cellulaire (mort et division cellulaires, qui partagent certaines caractéristiques morphologiques).Cette thèse propose une méthode intégrant de l'apprentissage automatique profond par réseau de neurones et du traitement de l'image et du signal afin d'effectuer des analyses de réponses cellulaires en utilisant l'imagerie dynamique de cellules uniques dans des expériences de profilage pharmacologique d'anticancéreux. Cette méthode procède par suivi automatique des cellules, extraction de caractéristiques cellulaires radiométriques et morphologiques, et analyse de l'évolution de ces caractéristiques au cours du temps pour chaque cellule afin de détecter des événements tels que la division et la mort cellulaire ainsi que d'enregistrer des dynamiques de signalisation cellulaire.Un cas d'étude comprenant l'analyse des dynamiques en cellules uniques de l'activité caspase-8 et de différentes caractéristiques cellulaires impactées par le traitement anticancéreux est présenté. L'objectif est de réaliser automatiquement et à grande échelle les analyses nécessaires pour faire évoluer la méthode de prédiction des phénotypes cellulaires (Fateseq) disponible dans le laboratoire, et de l'appliquer à diverses lignées cellulaires cancéreuses d'un panel de lignées cellulaires cancéreuses humaines afin d'améliorer les approches de profilage OMICS sur cellules vivantes et, à plus long terme, d'intensifier le criblage pharmacologique de nouveaux médicaments anticancéreux
Cell division and cell death are the main indicators to evaluate cancer drug action, and only their accurate measures can reveal the actual potency and efficacy of a compound. The detection of cell division and cell death events in live-cell assays has the potential to produce robust metrics of drug pharmacodynamics and return a more comprehensive understanding of tumor cells responses to cancer therapeutic combinations. Knowing precisely when a cell death or a cell division occurs in a live-cell experiment allows to study the relative contribution of different drug effects -such as cytotoxic or cytostatic effects, on a cell population. Yet, classical methods require dyes to measure cell viability as an end-point assay with whole population counts, where the proliferation rates can only be estimated when both viable and dead cells are labeled simultaneously.Live-cell imaging is a promising cell-based assay to determine drug efficacies, with the main limitation being the accuracy and depth of the analyses to detect and predict automatically cellular response phenotypes (cell death and division, which share some morphological features).This thesis introduces a method integrating deep learning using neural networks, and image and signal processing to perform dynamic image analyses of single-cell events in time-lapse microscopy experiments of drug pharmacological profiling. This method works by automatically tracking the cells, extracting radiometric and morphologic cell features, and analyzing the temporal evolution of these features for each cell so as to detect cellular events such as division and cell death, as well as acquiring signaling pathway dynamics.A case of study comprising the analyses of caspase-8 single-cell dynamics and other cell responses to cancer drugs is presented. The aim is to achieve automatically, at a large scale the necessary analyses to augment the phenotype prediction method available in the lab (Fateseq) and to apply it to various cancer cell lines of a human cancer cell line panel to improve our live-cell OMICS profiling approaches, and, in a longer term, to scale up pharmacological screening of new cancer drugs

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Green, Katherine J. "The effect of acute exercise on T-lymphocyte function". Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/36777/1/36777_Digitised%20Thesis.pdf.

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An increased incidence of illness has been observed in athletic populations undergoing intensive training and competition. T-lymphocytes are central to cell-mediated adaptive immune responses and have been the subject of many studies investigating the relationship between T-lymphocyte function, exercise and athlete health. A decrease in T-lymphocyte function following acute intensive exercise has commonly been described, making them a possible factor contributing to increased susceptibility in athlete populations. However, there is much controversy regarding the interpretation of traditional methodology (mitogen-induced proliferation assays) used to assess Tlymphocyte function during and after exercise. Current lymphocyte proliferation assays do not determine individual T-lymphocyte function or independently establish the function of T-lymphocyte subsets. Therefore, the overall aim of this thesis was to develop and apply new techniques to the study of the effect of acute exercise on the function of T-lymphocytes. Specifically, this thesis aimed to determine the effect of acute intensive exercise on the function of individual T-lymphocytes and T-lymphocyte subsets. The major findings of this thesis are that acute intensive exercise does impair Tlymphocyte responses to mitogen. The cellular expansion of both CD4 and CD8 Tlymphocytes as measured by the application of the new CFSE technique is decreased by acute exercise. The exercise effect observed is not an initial effect on cell function, as exercise does not impair the ability of T-lymphocytes to respond to stimulus (activation) and undergo cell division (mitosis) in response to mitogen. Instead, acute exercise is associated with an increased level of apoptosis in mitogen-stimulated cultures and this results in a reduction of the overall expansion of the cell population in vitro. The mechanism by which exercise induces apoptosis was examined using carbohydrate supplementation and it was found that carbohydrate feeding can prevent exercise-induced apoptosis, and hence attenuates the decrease in T-lymphocyte function. However, the mechanism by which carbohydrate prevents apoptosis does not appear to be via moderation of T-lymphocyte numbers or blood cortisol concentrations, rather it may be due to improved glucose availability.

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Pat, Sze Wa. "Cell metabolism in cell death and cell growth". HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.

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Dix, Christina Lyn. "Adhesion-dependent cell division". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044469/.

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Animal cells undergo a dramatic series of cell shape changes as they pass through mitosis and divide which depend both on remodelling of the contrac- tile actomyosin cortex and on the release of cell-substrate adhesions. Here, I use the adherent, non-transformed, human RPE1 cell line as a model system in which to explore the dynamics of these shape changes, and the function of mitotic adhesion remodelling. Although these cells are highly motile, and therefore polarised in interphase, many pause migration and elongate to be- come bipolar prior to mitosis. Interestingly, and in contrast to most reported cell types, these cells do not round fully, and many leave long adhesive tails con- nected to the underlying substrate. These are typically bipolar, persist through- out mitosis, and guide cell respreading following mitotic exit. Further analysis shows that while many proteins are lost from focal adhesion complexes during mitotic rounding, integrin-rich contacts remain in place along these tails as well as defining the tips of retraction fibres. These adhesions are functionally impor- tant in RPE1 cells, since these cells fail to divide when removed from the sub- strate prior to entry into mitosis. The restoration of cell-substrate adhesions at anaphase are sufficient to rescue division in control cells. However, adhesions must persist into mitotic exit for division in cells compromised in their ability to construct an actomyosin ring. Division in these cells depends on respreading, since Ect2 RNAi cells fail to divide on small adhesive islands, but successfully divide on larger patterns with the cytoplasmic bridge connecting daughter cells narrowing as they migrate away from one another. Together these results re- veal the importance of coupling adhesion remodeling to mitotic progression.

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Ellison, David William. "Cell proliferation, cell death, and differentiation in gliomas". Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295912.

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Crisby, Milita. "Cell death in atherosclerosis /". Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.

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Gorak-Stolinska, Patricia. "Activation induced cell death in human T cell subsets". Thesis, King's College London (University of London), 2002. http://kclpure.kcl.ac.uk/portal/en/theses/activation-induced-cell-death-in-human-t-cell-subsets(eb708e24-eccb-42fc-8930-d62ddf6794c1).html.

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RUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration". University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.

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Livros sobre o assunto "Cell division and cell death"

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Zirkin, Barry R., ed. Germ Cell Development, Division, Disruption and Death. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4.

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R, Zirkin B., Serono Symposia USA e Testis Workshop on Germ Cell Development, Division, Disruption, and Death (1997 : Baltimore, Md.), eds. Germ cell development, division, disruption, and death. Norwell, Mass: Serono Symposia USA, 1998.

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3

P, Studzinski George, ed. Cell growth, differentiation, and senescence: A practical approach. Oxford: Oxford University Press, 1999.

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Ockner, Robert K. Integration of metabolism, energetics, and signal transduction: Unifying foundations in cell growth and death, cancer, atherosclerosis, and Alzheimer disease. New York: Kluwer Academic Publishers, 2004.

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5

Melino, Gerry. Cell death. Chichester, UK: Wiley-Blackwell, 2010.

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Wu, Hao, ed. Cell Death. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9302-0.

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Gerry, Melino, e Vaux David, eds. Cell death. Chichester, West Sussex: John Wiley & Sons, 2010.

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Caillaud, Marie-Cécile, ed. Plant Cell Division. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1744-1.

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Macieira-Coelho, Alvaro, ed. Asymmetric Cell Division. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-69161-7.

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Caillaud, Marie-Cécile, ed. Plant Cell Division. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3142-2.

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Capítulos de livros sobre o assunto "Cell division and cell death"

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Campisi, Judith. "Cell Senescence and Aging". In Germ Cell Development, Division, Disruption and Death, 121–29. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_12.

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Knudson, C. Michael, Kenneth S. K. Tung e Stanley J. Korsmeyer. "Molecular Regulation of Testicular Cell Death". In Germ Cell Development, Division, Disruption and Death, 140–49. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_14.

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Swerdloff, Ronald S., YanHe Lue, Christina Wang, Tripathi Rajavashisth e Amiya Sinha Hikim. "Hormonal Regulation of Germ Cell Apoptosis". In Germ Cell Development, Division, Disruption and Death, 150–64. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_15.

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Tanaka, Hiromitsu, e Yoshitake Nishimune. "Cloning and Characterization of Genes Specifically Expressed in Germ Line Cells". In Germ Cell Development, Division, Disruption and Death, 3–10. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_1.

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Habener, Joel F., Philip B. Daniel e William H. Walker. "Expression of Activator and Repressor Isoforms of Transcription Factor CREB During Spermatogenesis". In Germ Cell Development, Division, Disruption and Death, 96–104. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_10.

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Braun, Robert E. "Repression and Activation of Protamine mRNA Translation During Murine Spermatogenesis". In Germ Cell Development, Division, Disruption and Death, 105–17. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_11.

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Chen, Haolin, Lindi Luo e Barry R. Zirkin. "Testicular Aging: Leydig Cells and Spermatogenesis". In Germ Cell Development, Division, Disruption and Death, 130–39. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_13.

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Sharpe, Richard M., Jane S. Fisher, Philippa T. K. Saunders, Gregor Majdic, Mike R. Millar, Priyanke Parte, Jeffrey B. Kerr e Katie J. Turner. "Estrogen Effects on Development and Function of the Testis". In Germ Cell Development, Division, Disruption and Death, 167–77. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_16.

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Kelce, William R., e Elizabeth M. Wilson. "Developmental Effects and Molecular Mechanisms of Environmental Antiandrogens". In Germ Cell Development, Division, Disruption and Death, 178–89. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_17.

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Robaire, Bernard, e Barbara F. Hales. "Targets of Chemotherapeutic Drug Action in Testis and Epididymis". In Germ Cell Development, Division, Disruption and Death, 190–201. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2206-4_18.

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Trabalhos de conferências sobre o assunto "Cell division and cell death"

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Li, Zhehan, David Grace e Paul Mitchell. "Cell division, migration and death for energy efficient 5G ultra-small cell networks". In 2014 IEEE Globecom Workshops (GC Wkshps). IEEE, 2014. http://dx.doi.org/10.1109/glocomw.2014.7063554.

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Beeharry, Neil, Xijun Zhu, Vignish Murali, Mitchell R. Smith e Timothy Yen. "Abstract A147: Pixantrone induces cell death through mitotic perturbations and subsequent aberrant cell divisions in solid tumor cell lines." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a147.

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Kraning-Rush, Casey M., Shawn P. Carey e Cynthia A. Reinhart-King. "Molded Collagen Microchannels for the Study of Cancer Cell Invasion". In ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icnmm2012-73093.

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Metastasis is the cause of 90% of cancer-related deaths and yet the precise mechanism of metastasis is poorly understood[1]. To metastasize, cells break free from the primary tumor, migrate through the surrounding tissue, and enter the vascular system to move to a secondary site. To migrate through the stroma, cell can both degrade the tissue and use physical force to move the tissue from its path. However, the relative roles of matrix degradation and cellular force are not well-understood. Previous work has shown that as cell move through the matrix, they create channels that other cells can then use to more easily escape from the primary tumor [2, 3]. To investigate the mechanisms by which metastatic cells move through 3D matrices, we fabricated microchannels from collagen that simulate the paths that are made and used by cells during metastasis. Here, we will present our method for molding channels in compliant collagen gels to investigate cell migration. The channels dimensions approximate the size of a cell and permit cell migration without the need for matrix degradation. We demonstrate that the channels cause persistent, unidirectional cell migration that is significantly faster than the migration observed in 3D matrices without channels. These channels provide a unique platform to probe 3D cellular migration and permit the dissection of the relative roles of matrix degradation and force generation in facilitating cell invasion.

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Ngo, Angela, Disha Sardana e Ivica Ico Bukvic. "Sonifying 2d Cellular Behavior Using Cellular Stethoscope". In ICAD 2022: The 27th International Conference on Auditory Display. icad.org: International Community for Auditory Display, 2022. http://dx.doi.org/10.21785/icad2022.015.

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This paper presents an approach to sonifying 2D cellular data. Its primary goal is attaining listener comprehension parity between original visual data and its sonified counterpart for the purpose of understanding cell behavior, including movement, mitosis (or division), and cell death. Here, we present the initial findings of the automated sonification prototype named “Cellular Stethoscope” that was assessed through a 19-subject pilot study to assess its ability to accurately reflect the cell behavior captured in the video footage. The resulting system is envisioned to serve as a foundation for a complementing and potentially more efficient approach to studying cell behavior when subjected to various pharmaceutical interventions.

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Hashimoto, Shigehiro. "Oblique Micro Grooves on Bottom Wall of Flow Channel to Sort Cells". In ASME 2020 Fluids Engineering Division Summer Meeting collocated with the ASME 2020 Heat Transfer Summer Conference and the ASME 2020 18th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/fedsm2020-20096.

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Abstract The movement of a flowing cell near the oblique micro groove on the bottom surface in the micro flow channel has been measured to sort biological cells in vitro. The micro groove of the rectangular shape (4.5 μm depth, and 0.2 mm length) was fabricated on the polydimethylsiloxane (PDMS) disk by the photolithography technique. The angle between the flow direction and the longitudinal axis of the groove is 45 degree. Variation has been made on the width (0.03 mm < w < 0.05 mm) of the groove. A rectangular flow channel (0.05 mm height × 1 mm width × 25 mm length) has been constructed between two transparent PDMS disks. C2C12 (mouse myoblast cell line) was used in the test. A flow velocity (0.1 mm/s < vx < 2.4 mm/s) of the suspension of cells was controlled by the pressure difference between the inlet and the outlet. The shifted distance of each cell along the oblique groove depends on the diameter of the cell. The malnourished cell with the different density can be distinguished by the shifted distance according to the velocity of the cell.

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Henkels, Julia A., e Evan A. Zamir. "A Novel Biomimetic Model for Studying Mechanics of Embryonic Morphogenesis and Differentiation". In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19608.

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Before the explosion of genetics research in the last century, embryonic development was largely studied from a mechanical perspective. Paired with genetic advances in understanding developmental signaling pathways and induction mechanisms, an important goal for understanding morphogenesis is to discover how the genome codes for changes in the mechanical movements of the embryonic cells. After formation of the zygote, a phase of rapid mitotic cell division is followed by epithelialization resulting in a cohesive sheet of cells termed the epiblast. During the next major phase of triploblastic development called gastrulation, a group of undifferentiated cells in the epiblast moves collectively to the embryonic midline and eventually gives rise to the three primary germ layers: endoderm, mesoderm, and ectoderm. At the primitive streak—the “organizing center” in amniotes (reptiles, birds, and mammals) which delineates anterior-posterior polarity—prospective endodermal and mesodermal precursors undergo epithelial-to-mesenchymal transition (EMT), internalization, and eventually organogenesis. “It is not birth, marriage, or death, but gastrulation which is truly the most important time in your life” (Lewis Wolpert, 1986).

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Hebeisen, Jason, Timothy M. Adams e Douglas Munson. "Sustained Pressure Test Results for Surface Scratches in PE4710, Cell Classification 445574C High Density Polyethylene Pipe Material". In ASME 2019 Pressure Vessels & Piping Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/pvp2019-93071.

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Abstract Mandatory Appendix XXVI of the ASME Boiler and Pressure Vessel Code (BPVC), Section III, Division 1 currently permits the use of high-density polyethylene (HDPE) in buried safety Class 3 piping systems. There have been concerns about how the slow crack growth (SCG) of HDPE emanating from surface scratches that may occur during fabrication or installation. The current allowable scratch depth in Appendix XXVI is 5% of the pipe wall thickness for pipe 4 inch and less in nominal diameter pipe and 0.040 inch (1mm) for pipe greater than 4 inch nominal diameter. This report presents the results of further investigation into the SCG rates by testing of notched PE 4710 HDPE pipes made from PE 4710 cell classification 445574C bimodal resins that meet the requirements of Appendix XXVI. These tests were conducted by first making razor-cut surface scratches in 4 inch, 8 inch, and 16 inch nominal diameter piping made by three different piping manufacturers using three different resins. The pipes were end-capped and pressure-tested at elevated temperature until failure, or until a prescribed number of test hours were reached. The razor cuts were at different depths and lengths so as to result in a variety of stress intensities, net section stresses, and nominal stresses. Following failure, or after the prescribed number of test hours was reached, the pipe specimens were inspected to determine the amount of SCG. This paper presents the results of the testing and recommended ASME BPVC Appendix XXVI changes for allowable crack depth based on the testing are provided.

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Richardson, William J., Dennis D. van der Voort e James E. Moore. "A Device to Subject Cells to Longitudinal Stretch Gradients on a Tube In Vitro". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80941.

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In the US, cardiovascular disease accounts for more than 800,000 deaths and an economic burden of nearly $300 billion per year. A major pathology afflicting the cardiovascular system is atherosclerosis, characterized by intraluminal plaque formation, producing a stenosis and obstructing flow. Balloon angioplasty, often coupled with the implantation of either a bare-metal or drug-eluting stent, has become a standard treatment of atherosclerosis. However, the host tissue’s response to stenting is frequently maladaptive, leading to intimal hyperplasia via smooth muscle cell (SMC) division and migration to the intima, and increased matrix protein synthesis, all contributing to restenosis of the vessel.

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9

Maeda, Noriyoshi, e Tetsuo Shoji. "Failure Probability Analysis by Probabilistic Fracture Mechanics Based on FRI SCC Model". In ASME 2010 Pressure Vessels and Piping Division/K-PVP Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/pvp2010-25917.

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Failure Probability of a weld by stress corrosion cracking (SCC) in austenitic stainless steel piping was analyzed by probabilistic fracture mechanics (PFM) approach based on electro-chemical crack growth model (FRI model). In this model, crack growth rate da/dt where a is crack depth is anticipated as the rate of chemical corrosion process defined by electro-chemical Coulomb’s law. The process is also related to the strain rate at the crack tip, taking small scale yielding condition into consideration. Derived transcendental equation is solved numerically by iterative method. Compared to the mechanical crack growth equation like Paris’ law for SCC, FRI model can introduce many electro-chemical parameters such as electric current associated with corrosion of newly born SCC crack surface, the frequency of protective film break and mechanical parameters such as stress intensity factor change with time dK/dt. Stratified Monte-Carlo method was introduced which define the cell of sampling space by the ranges of a/c (c is crack length at surface) and the width of K of sampling space, Kw which has to be defined referring to KSCC below which no SCC is caused. Log-normal distributions were anticipated for a/c distribution and K distribution. Parameter survey performed shows that failure probability which is defined as the ratio of crack number whose depth reached 80% of wall thickness to the total crack number depends on many parameters introduced, especially on yielding stress, electric current decay parameter m, strain hardening index n in Ramberg-Osgood equation and dK/dt. From the requirements of FRI model, two types of threshold value of initial crack depth, cracks having smaller depth than this value can not grow, are proposed. Calculated failure probability does not reach 1 when cracks having smaller initial depth than the threshold value are included in the distribution of analyzing cracks.

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10

Adams, Timothy M., Jason Hebeisen, Jie Wen e Douglas Munson. "Development of Crack Growth Curves and Correlation to Sustained Pressure Test Results for Cell Classification 445574C High Density Polyethylene Pipe Material". In ASME 2013 Power Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/power2013-98078.

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Code Case N755-1 of the ASME Boiler and Pressure Vessel Code, Section III, Division 1 Code currently permits the use of high density polyethylene (HDPE) in buried Safety Class 3 piping systems. There have been concerns with the Slow Crack Growth (SCG) of HDPE emanating from scratches that may occur during fabrication or installation. The possible use of tensile coupon tests for determining the life span of the pipe with surface scratches could provide a more cost effective testing method than does the use of sustained pressurized crack pipe tests. This paper presents the results of further investigation into the SCG rates of notched PE 4710 HDPE pipe made from a cell classification 445574C bimodal resin. The da/dt versus KI curves were developed from notched coupon testing. Standard fracture methods were then used to predict the failure time of the notched pressurized pipe specimens subjected to long-term hydraulic stress. The results for the SCG depth of the externally notched sustained pressurized pipe tests are provided along with the notched coupon test results. The actual failure times of the notched pressurized pipe tests are compared to the predicted failure times for the same specimens.

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Relatórios de organizações sobre o assunto "Cell division and cell death"

1

Baker, Nicholas E. Cell Proliferation, Cell Death, and Size Regulation. Fort Belvoir, VA: Defense Technical Information Center, outubro de 1998. http://dx.doi.org/10.21236/adb248354.

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2

Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, agosto de 1995. http://dx.doi.org/10.21236/ada300581.

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3

Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, outubro de 1997. http://dx.doi.org/10.21236/ada340671.

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4

Chung, Leland W. K. Accelerated Tumor Cell Death by Anglogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2005. http://dx.doi.org/10.21236/ada441865.

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5

Drews, Gary, N. Programmed Cell Death During Female Gametophyte Development. Office of Scientific and Technical Information (OSTI), setembro de 2004. http://dx.doi.org/10.2172/1014978.

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6

Chung, Leland W., Chia-Ling Hsieh, Michael Bradley e Mitchell H. Sokoloff. Accelerated Tumor Cell Death by Angiogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2001. http://dx.doi.org/10.21236/ada403672.

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7

Tyler, Kenneth L. Mechanisms of Virus-Induced Neural Cell Death. Fort Belvoir, VA: Defense Technical Information Center, março de 2005. http://dx.doi.org/10.21236/ada435392.

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8

Chung, Leland W. Accelerated Tumor Cell Death by Angiogenic Modifiers. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2003. http://dx.doi.org/10.21236/ada418654.

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9

Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, julho de 2012. http://dx.doi.org/10.21236/ada570124.

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10

Tyler, Kenneth L. Mechanisms of Virus-Induced Neural Cell Death. Fort Belvoir, VA: Defense Technical Information Center, setembro de 2003. http://dx.doi.org/10.21236/ada419455.

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