Relevant bibliographies by topics / Cell cycle

Academic literature on the topic 'Cell cycle'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Cell cycle"

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MACKEY, M. C. "The Cell Division Cycle: Cell Cycle Clocks." Science 227, no. 4691 (March 8, 1985): 1221. http://dx.doi.org/10.1126/science.227.4691.1221.

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Lavi, O., and Y. Louzoun. "What cycles the cell? -Robust autonomous cell cycle models." Mathematical Medicine and Biology 26, no. 4 (July 6, 2009): 337–59. http://dx.doi.org/10.1093/imammb/dqp016.

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Kornitskaya, Y. V., S. D. Bykova, and N. L. Gusakova. "Cell cycle." Тенденции развития науки и образования 96, no. 7 (2023): 106–8. http://dx.doi.org/10.18411/trnio-04-2023-366.

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The cell cycle is part of a general complex of processes that include ensuring the stability of the genetic material. If the cell cycle is disturbed, DNA synthesis is delayed, mitosis does not begin until the completion of replication, and is blocked in anaphase, if the attachment of chromosomes to the mitotic spindle is disturbed.
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Edgar, Bruce A. "Cell Cycle: Cell-cycle control in a developmental context." Current Biology 4, no. 6 (June 1994): 522–24. http://dx.doi.org/10.1016/s0960-9822(00)00113-5.

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Forsburg, Susan L. "Cell Cycle: In and out of the cell cycle." Current Biology 4, no. 9 (September 1994): 828–30. http://dx.doi.org/10.1016/s0960-9822(00)00184-6.

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Jacks, T. "CELL CYCLE: The Expanding Role of Cell Cycle Regulators." Science 280, no. 5366 (May 15, 1998): 1035–36. http://dx.doi.org/10.1126/science.280.5366.1035.

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Maddox, Amy Shaub, and Jan M. Skotheim. "Cell cycle, cell division, cell death." Molecular Biology of the Cell 30, no. 6 (March 15, 2019): 732. http://dx.doi.org/10.1091/mbc.e18-12-0819.

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Wells, D. N. "Keith's MAGIC: Cloning and the Cell Cycle." Cellular Reprogramming 15, no. 5 (October 2013): 348–55. http://dx.doi.org/10.1089/cell.2013.0038.

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Chia, Gloryn, and Dieter Egli. "Connecting the Cell Cycle with Cellular Identity." Cellular Reprogramming 15, no. 5 (October 2013): 356–66. http://dx.doi.org/10.1089/cell.2013.0041.

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Winey, Mark. "Cell cycle: Driving the centrosome cycle." Current Biology 9, no. 12 (June 1999): R449—R452. http://dx.doi.org/10.1016/s0960-9822(99)80279-6.

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Dissertations / Theses on the topic "Cell cycle"

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Chauhan, Anuradha. "Cell cycle." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16301.

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Die Zellreplikation ein kontrollierter Prozess aus sequentieller und zeitlich koordinierter Aktivierung und Abbau von Zyklinen, die einen schnellen Übergang zwischen den Zyklusphasen ermöglichen. Dabei ist der Erfolg bei der Ermittlung der wichtigsten Komponenten und Aufgliederung der Schaltmechanismen im Wesentlichen auf die gleichzeitige Anwendung von Modellsystemen wie Hefe, Frosch und Fliege zurückzuführen. Das heutige Verständnis des Zellzyklus muss erweitert werden, um zu überprüfen ob die Erkenntnisse auch auf in-vivo Modelle von Säugetieren wie der Maus zutreffen. Es existieren solche Modelle, die sich auf spezifische Kontrollpunkte oder Übergänge konzentrieren, allerdings noch kein integriertes Modell, in dem der Zellzyklus durch eine Verletzung im Säugetier induziert wird. Das Modellsystem der Leberregeneration bei Nagern wurde gewählt, da es sich durch das am höchsten verbreitete Phänomen der Synchronisation der Zellproliferation auszeichnet. Mit dem Fokus auf die Frage, wie die Zellen durch pro-inflammatorische Signale nach Verletzungen ins Priming in der G1/S Phase eintreten, gingen wir in einen durch Zytokine und Wachstumsfaktoren induzierten Säugetier-Zellzyklus über. Weiterhin wurden mitotische Ereignisse modelliert, die zum Alles-oder-Nichts G2/M Übergang und dem mitotischen Ausgang führen. Wir konzentrieren uns auf die vielversprechende Funktion von Cdh1 in der Zellzykluskontrolle, welches bekanntlich eine Schlüsselrolle in der G1 Phase spielt. Weiterhin haben wir dessen Rolle bei der Verzögerung der G2 Phase untersucht. Wir vermuten eine zentrale Rolle von Cdh1 im Zellzyklus durch die Kontrolle der Dynamik der Zykline. Das Modell ist ein Versuch, die Kernmechanismen der Zellzykluskontrolle bei Säugetieren zu verstehen. Besseres Verständnis der Mechanismen in der Säugetierzelle würde das Studium der Zellphysiologie im Hinblick auf Störungen der humanen Zellzyklusmaschinerie, welche zu Krankheiten wie Krebs führen.
Cell replication is a controlled process with sequential and timely activation and degradation of cyclins leading to swift transitions between the phases of the cell cycle. The essential achievement in identifying the key components and in dissecting the mechanisms of the cell cycle circuitry has been attributed to the simultaneous use of model systems like yeast, frogs, and flies. Present understanding of the cell cycle needs to be extended to investigate whether those findings also apply to mammalian in-vivo models like mice. We chose liver regeneration in mammals as the model system because it is the most synchronised cell proliferation phenomenon, where 95\% of the cells simultaneously enter cell cycle. The G1-S phase transition was modelled, focusing on how injury induced pro-inflammatory signals \textit{prime} the cells in G1 phase and consequently both cytokine and growth factor induced pathways lead to further cell cycle progression. The model was further extended to mitotic events leading to the all-or-none G2-M transition and mitotic exit. I focussed on the emerging role of Cdh1 in the mammalian cell cycle. Cdh1 known for its role in G1 phase was further investigated for its role G2 delay. Cdh1 was suggested to be at the core of the cell cycle machinery controlling cyclin dynamics. This model is an attempt in understanding core machinery of the mammalian cell cycle. Better understanding of the cell cycle control system in mammalian cells would enable understanding perturbations of the human cell cycle machinery which lead to diseases like cancers.
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Radmaneshfar, Elahe. "Mathematical modelling of the cell cycle stress response." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192232.

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Thanky, Niren Rasik. "The mycobacterial cell cycle." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405727.

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Chaffey, Gary S. "Modelling the cell cycle." Thesis, University of Surrey, 2015. http://epubs.surrey.ac.uk/807189/.

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This thesis may be divided into two related parts. The first of which considers a population balance approach to modelling a population of cells, with particular emphasis on how the cells pass between the G1 and S phases of the cell cycle. In the second part of the thesis a model is described which combines a cell cycle model with a simple Pharmacokinetic/Pharmacodynamic (PKPD) drug model. This model is then discussed in detail. Knowledge of how a population of cancerous cells progress through the cell cycle is vital if the population is to be treated effectively, as treatment outcome is dependent on the phase distributions of the population. Estimates on the phase distribution may be obtained experimentally however the errors present in these estimates may effect treatment efficacy and planning. In this thesis mathematical models are used to explore the factors that effect the phase distributions of the population. In this thesis it is shown that two different transition rates at the G1-S checkpoint provide a good fit to a growth curve obtained experimentally. However, the different transition functions predict a different phase distribution for the population, but both lying within the bounds of experimental error. Since treatment outcome is effected by the phase distribution of the population this difference may be critical in treatment planning. Using an age-structured population balance approach the cell cycle is modelled with particular emphasis on the G1-S checkpoint. By considering the probability of cells transitioning at the G1-S checkpoint, different transition functions are obtained. A suitable finite difference scheme for the numerical simulation of the model is derived and shown to be stable. The model is then fitted using the different probability transition functions to experimental data and the effects of the different probability transition functions on the model's results are discussed. In contrast to the population balance approach a more simplistic compartmental model is also considered. This model results in a system of linear ordinary differential equations which, under specific circumstances may be solved analytically. It is shown that whilst not as accurate as the population balance model this model provides an adequate fit to experimental data with the results for the total cell population lying within the bounds of experimental error. The ODE compartment model is combined with a simple PKPD model to allow a detailed analysis of the equations for this combined model to be undertaken for different drug-cell interactions. These results are then discussed. As a tumour grows many of the cells receive oxygen and nutrients from blood vessels formed within the tumour, these provide a less than ideal supply, resulting in areas that are well perfused, hypoxic and necrotic. In hypoxic regions the lack of oxygen and nutrients limit the cells' growth by increasing their cycle time and also reducing the effects of radiation and chemotherapy. In the conclusion of this thesis the idea of separating a tumour into three regions, normoxic, hypoxic and necrotic is discussed. Each of these regions may then be modelled using three coupled compartments, each of which contain a cell cycle model, modelled using a set of ordinary differential equations. Additionally, the interaction of a simple (PKPD) drug model with these populations of cells may be considered.
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Li, Victor Chun. "The Cell Cycle and Differentiation in Stem Cells." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10536.

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The relationship between cellular proliferation and differentiation is a major topic in cell biology. What we know comes from models of somatic cell differentiation, where it is widely viewed that cycling and differentiation are coupled, antagonistic phenomena linked at the G1 phase. The extension of this view to stem cells, however, is unclear. One potential possibility is that stem cells also tightly link their G1 phase with their differentiation, indicating a similarity between the differentiation of stem cells and the differentiation of more mature somatic cells. On the other hand, stem cells may utilize different mechanisms or adaptations that confer on them some aspect of uniqueness or "stemness." In this case, stem cells will not exhibit the same coupling with the cell cycle as in many somatic cell models. In this thesis, we examined mouse embryonic stem cells (mESCs), a stem cell that is pluripotent and rapidly cycling with a highly condensed G1 phase. Direct extension of the somatic view posits that elongation of their G1 phase to somatic lengths by cyclin-dependent kinase (CDK) activity inhibition should induce or increase differentiation of these stem cells. Evidence supporting this claim has been contradictory. We show that elongation of the cell cycle and elongation of G1 to somatic lengths is fully compatible with the pluripotent state of mESCs. Multiple methods that lengthen the cell cycle and that target CDK activity or that trigger putative downstream mechanisms (i.e. Rb and E2F activity) all fail to induce differentiation on their own or even to facilitate differentiation. These results indicates that the model of linkage between the G1 phase and differentiation in mESCs is incorrect and leads us to propose that "stemness" may have a physiological basis in the decoupling of cell cycling and differentiation. In summary, we provide evidence that there is a resistance of mESCs to differentiation induced by lengthening G1 and/or the cell cycle. This could allow for separate control of these events and provide new opportunities for investigation and application.
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Gauger, Michele Ann Sancar Aziz. "Cryptochrome, circadian cycle, cell cycle checkpoints, and cancer." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,971.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Dec. 18, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Biochemistry and Biophysics." Discipline: Biochemistry and Biophysics; Department/School: Medicine.
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Gad, Annica. "Cell cycle control by components of cell anchorage /." Stockholm : Division of Pathology, Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-359-0/.

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Cadart, Clotilde. "Cell size homeostasis in animal cells." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS103/document.

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Le mécanisme d’homéostasie de taille chez les cellules animales est très peu compris actuellement. Cette question est pourtant d’un intérêt majeur car le maintien de l’homéostasie de taille dans une population de cellules prolifératives doit se faire par une coordination entre la croissance et la division. Chez la levure S. pombe, il a ainsi été montré que la taille est une information cruciale pour déclencher l’entrée en mitose (Fantes, 1977). Chez plusieurs bactéries et les cellules filles de la levure S. cerevisiae au contraire, de récentes études ont au contraire montré que l’homéostasie de taille était le résultat d’une addition constante de volume, indépendamment de la taille initiale des cellules (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). Ce mécanisme est appelé « adder » et génère une régression des tailles à la moyenne, génération après génération. Ces résultats ont été possibles grâce au développement de techniques permettant la mesure dynamique du volume à l’échelle de la cellule unique et sur plusieurs générations. Une telle mesure est cependant très difficile chez les cellules de mammifère dont le volume fluctue constamment et qui cyclent sur des temps plus longs (environ 20 heures). Pour cette raison, la plupart des approches proposées sont indirectes (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) ou reposent sur une mesure de la masse plutôt que du volume (Mir et al. 2014; Son et al., 2012). Ensemble, ces études ont montré que les cellules de mammifère croissaient de manière exponentielle. Elles ont aussi remis en cause le modèle traditionnel qui proposait que l’homéostasie de taille reposait sur l’adaptation de la durée du cycle et mis en avant un rôle de la régulation de la vitesse de croissance. Cependant, aucun modèle n’a réellement été proposé ou démontré. La nature et l’existence même d’un mécanisme maintenant l’homéostasie de taille des cellules de mammifère est en fait discutée (Lloyd, 2013).Pour caractériser l’homéostasie de taille des cellules de mammifères, nous avons développé une technique permettant pour la première fois la mesure du volume de ces cellules sur des cycles complets (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). Nous montrons que plusieurs types cellulaires (HT29, MDCK et HeLa) se comportent d’une manière similaire à celle d’un « adder ». Pour tester davantage cette observation, nous induisons artificiellement des divisions asymétriques en confinant les cellules dans des micro-canaux. Nous observons que les asymétries de tailles sont réduites mais pas complètement corrigées au cours du cycle suivant, à la manière d’un « adder ». Pour comprendre comment la croissance et la progression dans le cycle sont coordonnées et génère cet « adder », nous combinons notre méthode de mesure de volume avec un suivi de la progression dans les différentes phases du cycle. Nous montrons que la durée de la phase G1 est inversement corrélée au volume initial des cellules. Cependant, cette corrélation semble contrainte par une durée minimale de G1 mise en évidence lors de l’étude de cellules artificiellement poussées à atteindre de grandes tailles. Néanmoins, même dans cette condition où la modulation de la durée du cycle est perdue, l’observation du « adder » est maintenue. Ceci suggère un rôle complémentaire de la régulation de la vitesse de croissance des cellules. Nous proposons donc une méthode pour estimer théoriquement la contribution relative de l’adaptation de la vitesse de croissance et de la durée du cycle dans le contrôle de la taille. Nous utilisons cette méthode pour proposer un cadre général où comparer le processus homéostatique des bactéries et de nos cellules. En conclusion, notre travail apporte pour la première fois la démonstration que les cellules de mammifères maintiennent l’homéostasie grâce à un mécanisme similaire au « adder ». Ce mécanisme semble impliquer à la fois une modulation de la durée du cycle et du taux de croissance
The way proliferating mammalian cells maintain a constant size through generations is still unknown. This question is however central because size homeostasis is thought to occur through the coordination of growth and cell cycle progression. In the yeast S. pombe for example, the trigger for cell division is the reach of a target size (Fantes, 1977). This mechanism is referred to as ‘sizer’. The homeostatic behavior of bacteria and daughter cells of the yeast S. cerevisiae on the contrary was recently characterized as an ‘adder’ where all cells grow by the same absolute amount of volume at each cell cycle. This leads to a passive regression towards the mean generation after generation (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). These findings were made possible by the development of new technologies enabling direct and dynamic measurement of volume over full cell cycle trajectories. Such measurement is extremely challenging in mammalian cells whose shape constantly fluctuate over time and cycle over 20 hours long periods. Studies therefore privileged indirect approaches (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) or indirect measurement of cell mass rather than cell volume (Mir et al. 2014; Son et al., 2012). These studies showed that cells overall grew exponentially and challenged the classical view that cell cycle duration was adapted to size and instead proposed a role for growth rate regulation. To date however, no clear model was reached. In fact, the nature and even the existence of the size homeostasis behavior of mammalian cells is still debated (Lloyd, 2013).In order to characterize the homeostatic process of mammalian cells, we developed a technique that enable measuring, for the first time, single cell volume over full cell cycle trajectories (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). We found that several cell types, HT29, HeLa and MDCK cells behaved in an adder-like manner. To further test the existence of homeostasis, we artificially induced asymmetrical divisions through confinement in micro-channels. We observed that asymmetries of sizes were reduced within the following cell cycle through an ‘adder’-like behavior. To then understand how growth and cell cycle progression were coordinated in way that generates the ‘adder’, we combined our volume measurement method with cell cycle tracking. We showed that G1 phase duration is negatively correlated with initial size. This adaptation is however limited by a minimum duration of G1, unraveled by the study of artificially-induced very large cells. Nevertheless, the adder behavior is maintained even in the absence of time modulation, thus suggesting a complementary growth regulatory mechanism. Finally, we propose a method to estimate theoretically the relative contribution of growth and timing modulation in the overall size control and use this framework to compare our results with that of bacteria. Overall, our work provides the first evidence that proliferating mammalian cells behave in an adder-like manner and suggests that both growth and cell cycle duration are involved in size control
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Poplawski, Andrzej. "Cell cycle analysis of archaea." Doctoral thesis, Uppsala University, Department of Cell and Molecular Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1078.

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In my thesis, the cell cycle analysis of archaea and hyperthermophilic organisms is presented for the first time. Crenarchaea from the genus Sulfolobus were used as a model system. Plow cytometry and light microscopy were applied to investigate the timing and coordination of different cell cycle events. Furthermore, DNA content, nucleoid structure, and nucleoid distribution at different stages during the cell cycle were studied. The Sulfolobus cell cycle was characterized as having a short pre-replication and a long post-replication period. The presence of a low proportion of cells with segregated genomes in the exponentially growing population suggested 3 considerable time delay between termination of chromosome replication and completion of nucleoid partition, reminiscent of the G2 period in eukaryotic cells.

The first available collection of conditional-lethal mutants of any archaeon or hyperthemophile was used to elucidate the coordination of cell cycle events. The studies showed that chromosome replication, nucleoid partition and cell division in Sulfolobus acidocaldarius, which are normally tightly coordinated during cellular growth, could be separately inhibited or uncoupled by mutation.

The ftsZ gene, which is involved in cell division in bacteria and euryarchaea, was isolated from the halophilic archaeon Haloferax mediterranei. Transcriptional start sites were mapped, and putative translation initiation elements were identified. In both the upstream and downstream regions of the ftsZ gene, open reading frames were found to be conserved within the genus Haloferax. Furthermore, at the 3' end of the ftsZ gene, the homologs of the bacterial secE and nusG genes are conserved in almost all euryarchaea analyzed so far. The studies also demonstrated the functional conservation of the FtsZ protein in different archaeal species, as well as between euryarchaea and bacteria.

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Shirazi, Fard Shahrzad. "The Heterogenic Final Cell Cycle of Retinal Horizontal Cells." Doctoral thesis, Uppsala universitet, Medicinsk utvecklingsbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-222559.

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The cell cycle is a highly complex process that is under the control of several pathways.  Failure to regulate and/or complete the cell cycle often leads to cell cycle arrest, which may be followed by programmed cell death (apoptosis). One cell type that has a variety of unique cell cycle properties is the horizontal cell of the chicken retina. In this thesis we aimed to characterize the final cell cycle of retinal horizontal cells. In addition, the regulation of the cell cycle and the resistance to apoptosis of retinal horizontal cells are investigated. Our results show that the final cell cycle of Lim1-expressing horizontal progenitor cells is heterogenic and three different cell cycle behaviors can be distinguished. The horizontal cells are generated by: (i) an interkinetic nuclear migration with an apical mitosis; (ii) a final cell cycle with an S-phase that is not followed by mitosis, such cells remain with a fully or partially replicated genome; or (iii) non-apical (basal) mitoses. Furthermore, we show that the DNA damage response pathway is not triggered during the heterogenic final cell cycle of horizontal progenitor cells. However, chemically induced DNA damage activated the DNA damage response pathway without leading to cell cycle arrest, and the horizontal progenitor cells entered mitosis in the presence of DNA damage. This was not followed by apoptosis, despite the horizontal cells being able to functionally activate p53, p21CIP1/waf1, and caspase-3. Finally, we show that FoxN4 is expressed in horizontal progenitor cells and is required for their generation. Over-expression of FoxN4 causes cell death in several neuronal retinal cell types, except horizontal cells, where it results in an overproduction. In conclusion, in this thesis, a novel cell cycle behavior, which includes endoreplication not caused by DNA damage and a basal mitosis that can proceed in the presence of DNA damage, is described. The cell cycle and cell survival processes are of particular interest since retinal horizontal cells are suggested to be the cell-of-origin for retinoblastoma.
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Books on the topic "Cell cycle"

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Pippa, Cristina. Cell cycle. Burlington, MA]: JAC Pub. & Promotions, 2007.

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A, Bryant J., and Francis D, eds. The eukaryotic cell cycle. New York: Taylor & Francis, 2008.

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1943-, Hunt Tim, ed. The cell cycle: An introduction. New York: W.H. Freeman, 1993.

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Murray, Andrew Wood. The cell cycle: An introduction. New York: Oxford University Press, 1993.

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Enders, Greg H. Cell cycle deregulation in cancer. New York: Springer, 2010.

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Humphrey, Tim, and Gavin Brooks. Cell Cycle Control. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592598579.

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Manfredi, James J., ed. Cell Cycle Checkpoints. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1217-0.

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Coutts, Amanda S., and Louise Weston, eds. Cell Cycle Oscillators. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1538-6.

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Wang, Zhixiang, ed. Cell-Cycle Synchronization. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2736-5.

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Banfalvi, Gaspar, ed. Cell Cycle Synchronization. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6603-5.

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Book chapters on the topic "Cell cycle"

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Takahashi, Naoki, and Masaaki Umeda. "Cell Cycle." In Cell Biology, 1–19. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7881-2_11-1.

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Nahler, Gerhard. "cell cycle." In Dictionary of Pharmaceutical Medicine, 23. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-89836-9_173.

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Csikász-Nagy, Attila. "Cell Cycle." In Encyclopedia of Systems Biology, 220–31. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_115.

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Adlung, Lorenz. "Cell Cycle." In Cell and Molecular Biology for Non-Biologists, 75–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65357-9_7.

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Mira, Grdisa, and Ana-Matea Mikecin. "Cell Cycle." In New Frontiers in Nanochemistry, 85–89. Includes bibliographical references and indexes. | Contents: Volume 1. Structural nanochemistry – Volume 2. Topological nanochemistry – Volume 3. Sustainable nanochemistry.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9780429022951-5.

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Siudeja, Katarzyna, Jannie de Jong, and Ody C. M. Sibon. "Studying Cell Cycle Checkpoints Using Drosophila Cultured Cells." In Cell Cycle Checkpoints, 59–73. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_6.

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Nikaido, Toshio, Koji Ono, Masuji Yamamoto, Toshiyuki Sakai, and Yasushi Magami. "Cell Cycle Regulation in Normal Versus Leukemic T Cells." In The Cell Cycle, 347–57. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_41.

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Kohn, Kurt W., Patrick M. O’Connor, and Joany Jackman. "Cell Cycle Regulation and the Chemosensitivity of Cancer Cells." In The Cell Cycle, 379–88. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_44.

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Behl, Christian, and Christine Ziegler. "Cell Cycle: The Life Cycle of a Cell." In Cell Aging: Molecular Mechanisms and Implications for Disease, 9–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-45179-9_2.

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Quaranta, Vito, Darren Tyson, and Peter Frick. "Cell Cycle, Cancer Cell Cycle and Oncogene Addiction." In Encyclopedia of Systems Biology, 341–43. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_49.

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Conference papers on the topic "Cell cycle"

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Gurkan-Cavusoglu, Evren, Jane E. Schupp, Timothy J. Kinsella, and Kenneth A. Loparo. "Analysis of cell cycle dynamics using probabilistic cell cycle models." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6089914.

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Spitzley, David V., Tiffany A. Brunetti, and Bruce W. Vigon. "Assessing Fuel Cell Power Sustainability." In Total Life Cycle Conference and Exposition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2000. http://dx.doi.org/10.4271/2000-01-1490.

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Stephenson, Dawn, and Ian Ritchey. "Parametric Study of Fuel Cell and Gas Turbine Combined Cycle Performance." In ASME 1997 International Gas Turbine and Aeroengine Congress and Exhibition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/97-gt-340.

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A number of cycles have been proposed in which a solid oxide fuel cell is used as the topping cycle to a gas turbine, including those recently described by Beve et al. (1996). Such proposals frequently focus on the combination of particular gas turbines with particular fuel cells. In this paper, the development of more general models for a number of alternative cycles is described. These models incorporate variations of component performance with key cycle parameters such as gas turbine pressure ratio, fuel cell operating temperature and air flow. Parametric studies are conducted using these models to produce performance maps, giving overall cycle performance in terms of both gas turbine and fuel cell design point operating conditions. The location of potential gas turbine and fuel cell combinations on these maps is then used to identify which of these combinations are most likely to be appropriate for optimum efficiency and power output. It is well known, for example, that the design point of a gas turbine optimised for simple cycle performance is not generally optimal for combined cycle gas turbine performance. The same phenomenon may be observed in combined fuel cell and gas turbine cycles, where both the fuel cell and the gas turbine are likely to differ from those which would be selected for peak simple cycle efficiency. The implications of this for practical fuel cell and gas turbine combined cycles and for development targets for solid oxide fuel cells are discussed. Finally, a brief comparison of the economics of simple cycle fuel cells, simple cycle gas turbines and fuel cell and gas turbine combined cycles is presented, illustrating the benefits which could result.
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Coulson, Guy, and Richard Stobart. "Life–Cycle Analysis and the Fuel Cell Car." In Total Life Cycle Conference and Exposition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2000. http://dx.doi.org/10.4271/2000-01-1485.

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Schneider, Eugenia, and Michael Mangold. "Problems During Cell Cycle in Artificial Cell Modeling." In Artificial Life 14: International Conference on the Synthesis and Simulation of Living Systems. The MIT Press, 2014. http://dx.doi.org/10.7551/978-0-262-32621-6-ch110.

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Schneider, Eugenia, and Michael Mangold. "Problems During Cell Cycle in Artificial Cell Modeling." In Artificial Life 14: International Conference on the Synthesis and Simulation of Living Systems. The MIT Press, 2014. http://dx.doi.org/10.1162/978-0-262-32621-6-ch110.

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Pascalie, Jonathan, Valérie Lobjois, Hervé Luga, Bernard Ducommun, and Yves Duthen. "Checkpoint oriented cell-cycle simulation." In the fourteenth international conference. New York, New York, USA: ACM Press, 2012. http://dx.doi.org/10.1145/2330784.2330966.

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Azizi, Aydin, and Navid Seifipour. "Modeling and Control of Cell Cycle." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163070.

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Faltenbacher, M., M. Betz, and P. Eyerer. "Alternative Fuels for Fuel Cell Powered Buses in Comparison to Diesel powered Buses." In Total Life Cycle Conference and Exposition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2000. http://dx.doi.org/10.4271/2000-01-1484.

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Saito, Norihiko, Nozomi Hirai, Kazuya Aoki, Satoshi Fujita, Haruo Nakayama, Morito Hayashi, Takatoshi Sakurai, and Satoshi Iwabuchi. "Abstract 2621: OLIG2 regulates stem cell maintenance and cell cycle in glioma stem cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2621.

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Reports on the topic "Cell cycle"

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Williams, Thomas. Cell Biology Board Game: Cell Life Cycle Top Trumps. University of Dundee, January 2023. http://dx.doi.org/10.20933/100001277.

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All living things from whole people to single cells and even viruses have life cycles. Explore the weird and wonderful world of life cycles at the level of the cell in this top trumps inspired game. Print and cut out the cards, then play anywhere you want!
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Reed, Steven I. Cell Cycle in Normal and Malignant Breast Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada315811.

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Reed, Steven I. Cell Cycle in Normal and Malignant Breast Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada300387.

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Reed, Steven I. Cell Cycle in Normal and Malignant Breast Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada354074.

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Dooner, Mark, Jason M. Aliotta, Jeffrey Pimental, Gerri J. Dooner, Mehrdad Abedi, Gerald Colvin, Qin Liu, Heinz-Ulli Weier, Mark S. Dooner, and Peter J. Quesenberry. Cell Cycle Related Differentiation of Bone Marrow Cells into Lung Cells. Office of Scientific and Technical Information (OSTI), December 2007. http://dx.doi.org/10.2172/936517.

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McConkey, David J. Cell Cycle Dependence of TRAIL Sensitivity in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada466697.

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McConkey, David J. Cell Cycle Dependence of TRIAL Sensitivity in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada481365.

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Rich, Alexander. Transcriptional Regulation in the Cell Cycle. Fort Belvoir, VA: Defense Technical Information Center, October 1988. http://dx.doi.org/10.21236/ada200715.

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Chaney, Larry J., Mike R. Tharp, Tom W. Wolf, Tim A. Fuller, and Joe J. Hartvigson. FUEL CELL/MICRO-TURBINE COMBINED CYCLE. Office of Scientific and Technical Information (OSTI), December 1999. http://dx.doi.org/10.2172/802823.

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Kuhne, Wendy, Candace Langan, Lucas Angelette, and Lesleyann Hawthorne. Deuterium Concentration Effects on Cell Cycle Progression. Office of Scientific and Technical Information (OSTI), August 2020. http://dx.doi.org/10.2172/1651107.

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