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Relevant bibliographies by topics / Cell division. Cell cycle

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Academic literature on the topic 'Cell division. Cell cycle'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "Cell division. Cell cycle"

1

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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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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Coller, Hilary A., and Arshad Desai. "Cell cycle, cell division, and cell death." Molecular Biology of the Cell 28, no. 6 (March 15, 2017): 693–94. http://dx.doi.org/10.1091/mbc.e16-11-0793.

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Pennisi, E. "CELL CYCLE: Cell Division Gatekeepers Identified." Science 279, no. 5350 (January 23, 1998): 477–78. http://dx.doi.org/10.1126/science.279.5350.477.

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Sun, Jing, Run Shi, Sha Zhao, Xiaona Li, Shan Lu, Hemei Bu, and Xianghua Ma. "Cell division cycle 45 promotes papillary thyroid cancer progression via regulating cell cycle." Tumor Biology 39, no. 5 (May 2017): 101042831770534. http://dx.doi.org/10.1177/1010428317705342.

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Cell division cycle 45 was reported to be overexpressed in some cancer-derived cell lines and was predicted to be a candidate oncogene in cervical cancer. However, the clinical and biological significance of cell division cycle 45 in papillary thyroid cancer has never been investigated. We determined the expression level and clinical significance of cell division cycle 45 using The Cancer Genome Atlas, quantitative real-time polymerase chain reaction, and immunohistochemistry. A great upregulation of cell division cycle 45 was observed in papillary thyroid cancer tissues compared with adjacent normal tissues. Furthermore, overexpression of cell division cycle 45 positively correlates with more advanced clinical characteristics. Silence of cell division cycle 45 suppressed proliferation of papillary thyroid cancer cells via G1-phase arrest and inducing apoptosis. The oncogenic activity of cell division cycle 45 was also confirmed in vivo. In conclusion, cell division cycle 45 may serve as a novel biomarker and a potential therapeutic target for papillary thyroid cancer.

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Gutierrez, Crisanto. "The Arabidopsis Cell Division Cycle." Arabidopsis Book 7 (January 2009): e0120. http://dx.doi.org/10.1199/tab.0120.

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Salazar-Roa, María, and Marcos Malumbres. "Fueling the Cell Division Cycle." Trends in Cell Biology 27, no. 1 (January 2017): 69–81. http://dx.doi.org/10.1016/j.tcb.2016.08.009.

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Gichner, T. "The cell division cycle in plants." Biologia Plantarum 28, no. 2 (March 1986): 148. http://dx.doi.org/10.1007/bf02885216.

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Bray, C. M. "The Cell Division Cycle in Plants." FEBS Letters 219, no. 2 (July 27, 1987): 492. http://dx.doi.org/10.1016/0014-5793(87)80285-5.

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Pryke, J. A. "The cell division cycle in plants." Endeavour 10, no. 1 (January 1986): 55. http://dx.doi.org/10.1016/0160-9327(86)90079-7.

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Dissertations / Theses on the topic "Cell division. Cell cycle"

1

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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Jacob, Cara. "cdca8 : a target of p53/Rb dependent repression /." See Full Text at OhioLINK ETD Center (Requires Adobe Acrobat Reader for viewing), 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1114615830.

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Carvalhal, Sara. "Characterisation of ALADIN's function during cell division." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/cb6fe2ac-a17b-487e-ae16-a646e6576534.

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Cell division relies on many steps, precisely synchronised, to ensure the fidelity of chromosome segregation. To achieve such complex and multiple functions, cells have evolved mechanisms by which one protein can participate in numerous events on the cell life. Over the past few years, an increasing number of functions have been assigned to the proteins of the nuclear pore complex (NPC) also called nucleoporins. NPCs are large complexes studded in the nuclear envelope, which control the nucleocytoplasmic transport. It is now known that nucleoporins participate in spindle assembly, kinetochore organisation, spindle assembly checkpoint, and all processes important for genome integrity maintenance. This work demonstrates that the nucleoporin ALADIN participates in mitosis, meiosis and in cilia. In both mitosis and meiosis, ALADIN is important for proper spindle assembly. In mitosis, it was also discovered that ALADIN is a novel factor in the spatial regulation of the mitotic regulator Aurora A kinase. Without ALADIN, active Aurora A spreads from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. Interestingly, mutations in ALADIN causes triple A syndrome and some of the mitotic phenotypes observed after ALADIN depletion also occur in cells from triple A syndrome patients. In meiosis, ALADIN contributes to trigger the resumption of meiosis in female mouse. Impairment of ALADIN from mouse oocyte slows spindle assembly, migration and reduces oocytes ability to extrude polar bodies during meiosis I, which concomitantly affects the robustness of oocyte maturation and impairs mouse embryo development. Nucleoporins were also found at the base of the cilia, a centriole-derived organelle that participates in differentiation, migration, cell growth from development to adulthood. Here it is shown that ALADIN is also localised at the base of the cilia. With this work, new ALADIN’s functions have been identified across cell division, as well as uncovered an unexpected relation between triple A syndrome and cell division.

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Wang, Yan. "Characterization of the effects of decreased expression of ribosomal proteins on cell transformation and cell cycle regulation." Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/11190.

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Lundgren, Magnus. "Exploring the Cell Cycle of Archaea." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7848.

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Keifenheim, Daniel L. "Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/784.

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The coordination between cell growth and division is a highly regulated process that is intimately linked to the cell cycle. Efforts to identify an independent mechanism that measures cell size have been unsuccessful. Instead, we propose that size control is an intrinsic function of the basic cell cycle machinery. My work shows that in the fission yeast Schizosaccharomyces pombe Cdc25 accumulates in a size dependent manner. This accumulation of Cdc25 occurs over a large range of cell sizes. Additionally, experiments with short pulses of cycloheximide have shown that Cdc25 is an inherently unstable protein that quickly returns to a size dependent equilibrium in the cell suggesting that Cdc25 concentration is dependent on size and not time. Thus, Cdc25 can act as a sizer for the cell. However, cells are still viable when Cdc25 is constitutively expressed suggesting that there is another sizer in the case that Cdc25 expression is compromised. Cdc13 is a likely candidate due to the similar characteristics to Cdc25 and the ability to activate Cdc2. Cdc13 accumulates during the cell cycle in a manner similar to Cdc25. I show that in the absence of Cdc2 tyrosine phosphorylation, the cell size is sensitive to Cdc13 activity showing that Cdc13 accumulation can determine when cells enter mitosis. These results suggest a two sizer model where Cdc25 is the main sizer with Cdc13 acting as a backup sizer in the event of Cdc25 expression is compromised. Additionally, in the absence of Cdc2 phosphorylation by the kinases Wee1 and Mik1, mitotic entry is regulated by the activity of Cdc2. In the absence of Cdc2 phosphorylation, this activity is regulated by binding of cyclins to Cdc2. Under these circumstances, the activity of Cdc13 can regulate mitotic entry provide further evidence that Cdc13 could be a sizer of the cell in the case where Cdc25 expression is compromised. The results I present in this dissertation provide the groundwork for understanding how cells regulate size and how this size regulation affects cell cycle control in S. pombe . The results show how the intrinsic cell cycle machinery can act as a sizer for the G2/M transition in S. pombe . Interestingly, this mitotic commitment pathway is well conserved suggesting a general solution for size control in eukaryotes at the G2/M transition. Understanding the mechanism of how protein concentration is regulated in a size dependent manner will give much needed insight into how cells control size. Elucidating the mechanism for size control will capitalize on decades of research and deepen our understanding of basic cell biology.

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Huang, Yu-Ting. "The regulatory role of Pax6 on cell division cycle associated 7 and cortical progenitor cell proliferation." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29573.

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Forebrain development is controlled by a set of transcription factors which are expressed in dynamic spatiotemporal patterns in the embryonic forebrain and are known to regulate complex gene networks. Pax6 is a transcription factor that regulates corticogenesis and mutations affecting Pax6 protein levels cause neurodevelopmental defects in the eyes and forebrain in both humans and mice. In previous studies, it was shown that the graded expression pattern of Pax6 protein, which is high rostro-laterally to low caudo-medially in the cerebral cortex, is critical for its control of cell cycle progression and proliferation of cortical progenitors. However the underlying mechanisms are still unclear. Based on a microarray analysis carried out in our laboratory, a number of cell cycle-related candidate genes that may be affected by Pax6 have been identified. One such gene, Cell division cycle associated 7 (Cdca7) is expressed in a counter-gradient against that of Pax6. In my current study, I found that Cdca7 mRNA expression in the telencephalon is upregulated in Pax6 null (Small eye) mutants and downregulated in mice that overexpress PAX6 (PAX77) across developing time points from E12.5 to E15.5. There are several potential Pax6 binding motifs located in the genomic locus upstream of Cdca7. However, by chromatin immunoprecipitation, it is showed that none of the predicted binding sites are physically bound by Pax6. Promoter luciferase assays using fragments combining five suspected binding motifs show that Pax6 is functionally critical. Cdca7 is also identified as a Myc and E2F1 direct target and is upregulated in some tumours but its biological role is not fully understood. Current work using in utero electroporation to overexpress Cdca7 around the lateral telencephalon, where Cdca7 expression levels are normally low, tested the effects on the proliferation and differentiation of cortical progenitor cells in this region. In E12.5 mice embryos, overexpression of Cdca7 protein causes fewer intermediate progenitor cells and post-mitotic neurons to be produced but these effects were not found in E14.5 embryos. This result implies that Cdca7 may affect cell fate decision during cortical development.

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Shorter, James Gordon. "Molecular mechanisms regulating Golgi architecture during the mammalian cell division cycle." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313395.

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Giunta, Simona. "DNA damage responses in the context of the cell division cycle." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/228687.

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During my PhD, I have investigated aspects of the DNA damage response (DDR) in the context of three different cellular scenarios: DNA damage signalling in response to double-strand breaks during mitosis, coordination of DNA replication with DNA damage responses by regulation of the GINS complex, and checkpoint activation by the prototypical checkpoint protein Rad9. Here, I show that mitotic cells treated with DNA break-inducing agents activate a 'primary' DDR, including ATM and DNA-PK-dependent H2AX phosphorylation and recruitment of MDC1 and the MRN complex to damage sites. However, downstream DDR events and induction of a DNA damage checkpoint are inhibited in mitosis, with full DDR activation only ensuing when damaged mitotic cells enter G1. In addition, I provide evidence that induction of a primary DDR in mitosis is biologically important for cell viability. The GINS complex is an evolutionarily conserved component of the DNA replication machinery and may represent an ideal candidate for transferring the DNA damage signal to the replication apparatus. Here, I show the identification of a consensus 'SQ' PIKK phosphorylation motif at the carboxyl end of the GINS complex subunit, Psf1. In Saccharomyces cerevisiae, switching the conserved serine to a glutamic acid is lethal, indicating that the site is crucial for the protein's function. Moreover, in human cells, I identified UV-DDB, a heterodimeric complex involved in NER repair, as a binding partner that specifically interacts with the Psf1 C-terminus in vitro. Finally, I discuss my findings in characterizing functional interactions between Rad9 and Chk1 in S. cerevisiae. I show that specific consensus CDK sites within Rad9 N-terminus are essential to enable Chk1 phosphorylation and activation, and that MCPH1, a human homologue of Rad9, may share a conserved function in binding and activating Chk1, underscoring the evolutionarily conservation of checkpoint activation mechanisms.

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Jurczyk, Agata. "Centrosomes in Cytokinesis, Cell Cycle Progression and Ciliogenesis: a Dissertation." eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/73.

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The work presented here describes novel functions for centrosome proteins, specifically for pericentrin and centriolin. The first chapter describes the involvement of pericentrin in ciliogenesis. Cells with reduced pericentrin levels were unable to form primary cilia in response to serum starvation. In addition we showed novel interactions between pericentrin, intraflagellar transport (IFT) proteins and polycystin 2 (PC2). Pericentrin was co-localized with IFT proteins and PC2 to the base of primary cilia and motile cilia. Ciliary function defects have been shown to be involved in many human diseases and IFT proteins and PC2 have been implicated in these diseases. We conclude that pericentrin is required for assembly of primary cilia possibly as an anchor for other proteins involved in primary cilia assembly. The second chapter describes identification of centriolin, a novel centriolar protein that localizes to subdistal appendages and is involved in cytokinesis and cell cycle progression. Depletion of centriolin leads to defects in the final stages of cytokinesis, where cells remain connected by thin intercellular bridges and are unable to complete abscission. The cytokinesis defects seemed to precede the G0/G1 p53 dependant cell cycle arrest. Finally, the third chapter is a continuation of the cytokinesis study and it identifies pericentrin as an interacting partner for centriolin. Like centriolin, pericentrin knockdown induces defects in the final stages of cytokinesis and leads to G0/G1 arrest. Moreover, pericentrin and centriolin interact biochemically and show codependency in their centrosome localization. We conclude that pericentrin and centriolin are members of the same pathway and are necessary for the final stages of cytokinesis.

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Books on the topic "Cell division. Cell cycle"

1

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

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The cell cycle: Principles of control. London: Published by New Science Press in association with Oxford University Press, 2007.

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Transient processes in cell proliferation kinetics. Berlin: Springer-Verlag, 1989.

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Symposium, British Society for Cell Biology. The cell cycle: Proceedings of the British Society for Cell Biology-Journal of Cell Science Symposium, St Andrews, April 1989. Cambridge [Eng.]: Company of Biologists, 1989.

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The biology of cell reproduction. Cambridge, Mass: Harvard University Press, 1985.

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Goode, Jamie, Gregory Bock, and Gail Cardew. The cell cycle and development. New York: Wiley, 2001.

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Boonstra, Johannes. G1 phase progression. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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Lalonde, Jules A. Analysis of a biochemical reaction network that drives the eukaryotic cell division cycle. Sudbury, Ont: Laurentian University, 1996.

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Bacterial growth and division: Biochemistry and regulation of prokaryotic and eukaryotic division cycles. San Diego: Academic Press, 1991.

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

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Book chapters on the topic "Cell division. Cell cycle"

1

Carraway, Kermit L., Coralie A. Carothers Carraway, and Kermit L. Carraway. "Cell Cycle and Cell Division." In Signaling and the Cytoskeleton, 177–210. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-12993-7_5.

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D. Aguda, Baltazar. "Modeling the Cell Division Cycle." In Tutorials in Mathematical Biosciences III, 1–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11561606_1.

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Smaaland, Rune. "Circadian rhythm of cell division." In Progress in Cell Cycle Research, 241–66. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5873-6_23.

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Jenness, D. D., A. C. Burkholder, and L. H. Hartwell. "Hormonal Control of Cell Division in Saccharomyces cerevisiae." In Cell Cycle and Oncogenes, 24–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71686-7_3.

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Dawson, Scott C., Eva Nohýnková, and Michael Cipriano. "Cell Cycle Regulation and Cell Division in Giardia." In Giardia, 161–83. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0198-8_10.

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Pirincci Ercan, Deniz, and Frank Uhlmann. "Analysis of Cell Cycle Progression in the Budding Yeast S. cerevisiae." In Methods in Molecular Biology, 265–76. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1538-6_19.

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AbstractThe cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. In eukaryotes, cyclin–cyclin-dependent kinase (cyclin–Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. Their activity and expression profiles are regulated in time. The budding yeast S. cerevisiae was one of the pioneering model organisms to study the cell cycle. Its genetic amenability continues to make it a favorite model to decipher the principles of how changes in cyclin-Cdk activity translate into the intricate sequence of substrate phosphorylation events that govern the cell cycle. In this chapter, we introduce robust and straightforward methods to analyze cell cycle progression in S. cerevisiae. These techniques can be utilized to describe cell cycle events and to address the effects of perturbations on accurate and timely cell cycle progression.

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Pasternak, C. A. "Surface Changes in Relation to Cytokinesis and Other Stages During the Cell Cycle." In Biomechanics of Cell Division, 187–96. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1271-0_9.

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Vernoux, Teva, Daphné Autran, and Jan Traas. "Developmental control of cell division patterns in the shoot apex." In The Plant Cell Cycle, 25–37. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-010-0936-2_3.

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Hiramoto, Yukio. "Mechanical Properties of the Protoplasm of Echinoderm Eggs at Various Stages of Cell Cycle." In Biomechanics of Cell Division, 13–32. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1271-0_2.

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Baskin, Tobias I. "On the constancy of cell division rate in the root meristem." In The Plant Cell Cycle, 1–10. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-010-0936-2_1.

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Conference papers on the topic "Cell division. Cell cycle"

1

Bagui, Tapan K., Savitha Sharma, and W. J. Pledger. "Abstract 2953: Involvement of HDAC11 in cell division cycle." In 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.am2011-2953.

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Zoltowski, Mariusz L. "A Signal Processing Attempt to Identify Cell Division Cycle (CDC) m-RNAs Reveals Couplings with Other Cell Cycles." In Biomedical Engineering. Calgary,AB,Canada: ACTAPRESS, 2016. http://dx.doi.org/10.2316/p.2016.832-028.

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Govaerts, Willy, Virginie De Witte, and Leila Kheibarshekan. "Using MatCont in a Two-Parameter Bifurcation Study of Models for Cell Cycle Controls." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-86185.

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A recent application field of bifurcation theory is in modelling the cell cycle. We refer in particular to the work of J.J. Tyson and B. Novak where the fundamental idea is that the cell cycle is an alternation between two stable steady states of a system of kinetic equations. We study and extend the basic model of Tyson and Novak using the Matlab numerical bifurcation software MatCont, in a two-parameter setting and highlight several new features. We show that the limit point curves in the two-variable model behave in an ungeneric way under variation of the natural parameters and that the hysteresis loop in the model is not the usual loop caused by the existence of a codimension-2 cusp point. We continue orbits homoclinic-to-saddle-node (HSN) in the three-variable model and find that these orbits die in a non-central orbit homoclinic-to-saddle-node under a natural parameter variation. As an extension we introduce a model in which cell division appears as a continuous-in-time limit cycle. We perform a continuation of this limit cycle under a natural parameter variation and show that it loses stability in a limit point of cycles bifurcation. Alternatively, we study the cell cycle as a boundary value problem as proposed by Tyson and Novak. This leads to an interpretation of the cell as a slow-fast system and we derive several conclusions on the relation between the growth rate of the cells and the cell size at division, and on the controllability of the process.

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Fujino, Naoya, Toshifumi Fujimori, Rose Maciewicz, and Tracy Hussell. "Axl receptor tyrosine kinase drives cell cycle re-entry and promotes symmetric cell division of airway basal cells in response to injury." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa4980.

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Bailis, Julie, Li Fang, Jessica Orf, Scott Heller, Tammy Bush, Matthew Bourbeau, Sonia Escobar, et al. "Abstract 711: Small molecule compounds that target cell division cycle 7 (Cdc7) kinase inhibit cell proliferation and tumor growth." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-711.

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Tamburello, David, Bruce Hardy, Claudio Corgnale, Martin Sulic, and Donald Anton. "Cryo-Adsorbent Hydrogen Storage Systems for Fuel Cell Vehicles." In ASME 2017 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/fedsm2017-69411.

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Numerical models for the evaluation of cryo-adsorbent based hydrogen (H2) storage systems for fuel cell vehicles were developed and validated against experimental data. These models simultaneously solve the equations for the adsorbent thermodynamics together with the conservation equations for heat, mass, and momentum. The models also use real gas thermodynamic properties for hydrogen. Model predictions were compared to data for charging and discharging both activated carbon and MOF-5™ systems. Applications of the model include detailed finite element analysis simulations and full vehicle-level system analyses. The full system models were used to compare prospective system design performance given specific options, such as the adsorbent materials, pressure vessel types, internal heat exchangers, and operating conditions. The full vehicle model, which also allows the user to compare adsorbent systems with compressed gas, metal hydride, and chemical hydrogen storage systems, is based on an 80 kW fuel cell with a 20 kW battery evaluated using standard drive cycles. This work is part of the Hydrogen Storage Engineering Center of Excellence (HSECoE), which brings materials development and hydrogen storage technology efforts together to address onboard hydrogen storage in light duty vehicle applications. The HSECoE spans the design space of the vehicle requirements, balance of plant requirements, storage system components, and materials engineering. Theoretical, computational, and experimental efforts are combined to evaluate, design, analyze, and scale potential hydrogen storage systems and their supporting components against the Department of Energy (DOE) 2020 and Ultimate Technical Targets for Hydrogen Storage Systems for Light Duty Vehicles.

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VanOsdol, John, and Edward L. Parsons. "Using Staged Compression and Expansion to Enhance the Performance of a Gas Turbine Fuel Cell Hybrid System." In ASME 2009 7th International Conference on Fuel Cell Science, Engineering and Technology. ASMEDC, 2009. http://dx.doi.org/10.1115/fuelcell2009-85078.

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It has long been recognized that the heat generated from a solid oxide fuel cell (SOFC) is adequate to drive an external heat engine. The combination of the fuel cell plus the heat engine is called a gas turbine fuel cell hybrid power generation system. In most hybrid systems the heat engine consists of a single compressor and single turbine, arranged in either a Brayton cycle or a recuperated Brayton cycle. One characteristic of hybrid power cycles is that the compression costs are substantial. When this cycle is used in a coal fired hybrid system that is configured with an isolated anode stream to isolate and compress CO2, the work to compress the cathode air can greatly exceed the work to compress the CO2. It has also been shown for this same system that using intercooled compression for the cathode air reduces this compression cost. Since there have been no exhaustive studies performed which quantify these effects it is not clear exactly how much reduction in compression cost is possible. In this work we compare three hybrid systems. The first systems has a single compressor and turbine, run at a low pressure ratio as a recuperated Brayton cycle and at high pressure ratio as a simple Brayton cycle (see Figure 1). We then alter the recuperated Brayton cycle using both staged compression and staged expansion. The second system is thus configured with two compressors and two turbines. For this system an intercooler is placed between the compressors and the fuel cell stack is divided into two stacks each followed by a turbine (see Figure 3). Similarly the third system divides the compression and expansion legs of the cycle again into three compressors with intercoolers, and three fuel cell stacks each followed by its own turbine (see Figure 5). As the system configuration is altered by successive divisions of both the compression and expansion legs of the thermal heat engine cycle, the system configuration is transformed from a simple Brayton cycle to a staged approximation to an Ericsson cycle. We show that this new configuration for the gas turbine fuel cell hybrid system not only reduces the high cost of compression, but it makes more heat available for auxiliary system operations. In coal fired systems these auxiliary operations would include pre heating coal for the gasification system, reheating the syngas after cooling or even heating steam for a bottoming cycle.

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Hashimoto, Shigehiro. "Behavior of Myoblast Under Shear Stress in Couette Type of Flow." 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/fedsm2020-20075.

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Abstract Behavior of myoblast has been investigated under the uniform shear flow in vitro. The culture medium was sandwiched with the constant gap between the lower stationary culture plate and the upper rotating parallel plate to make a Couette type of the shear flow. By the rotating speed of the upper disk, the wall shear stress (τ) on the lower culture plate was controlled. C2C12 (mouse myoblast cell) was used in the test. After cultivation without flow for 24 hours for adhesion of cells on the lower plate, τ < 2 Pa was continuously applied on cells for 7 days in the incubator. Behavior of each cell was traced at the time lapse images observed by an inverted phase contrast microscope placed in an incubator. Experimental results show that cells differentiate to myotubes under τ < 2 Pa. Both the cell cycle and the cell length tend to scatter in the wider range, and the longitudinal axis of each cell tends to align to the flow direction by the shear stress of 1 Pa. The experimental system is useful to study quantitative relationships between the shear stress and the cell behavior: deformation, orientation, and differentiation.

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Kammerstätter, S., and T. Sattelmayer. "Influence of Prechamber-Geometry and Operating-Parameters on Cycle-to-Cycle Variations in Lean Large-Bore Natural Gas Engines." In ASME 2012 Internal Combustion Engine Division Spring Technical Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/ices2012-81180.

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Lean large-bore natural gas engines are usually equipped with gas-scavenged prechambers. After ignition and during combustion in the prechamber hot reacting jets penetrate the main chamber and provide much higher ignition energies than electric spark plugs. Although prechambers stabilize combustion, limitations of the concept are observed at very lean main chamber mixtures and large cylinder diameters, which appear as cycle-to-cycle variations of heat release and pressure. At the Thermodynamics Institute of the Technical University of Munich cycle-to-cycle variations are investigated in an unique periodically chargeable high pressure combustion cell with full optical access to the entire main chamber. Recently, the influence of the ignition timing, the amount of scavenge-gas of the prechamber and the cross section of the prechamber exit orifices on cycle-to-cycle variations have been studied. From the pressure traces characteristic parameters of the combustion process like the ignition probability, the ignition delay and the rate of the pressure rise have been derived. By analysing the emission of OH*-chemiluminescence in terms of reacting area and light emission and on the basis of numerical simulations information on the source of cycle-to-cycle variations is obtained. Finally it is shown that cycle-to-cycle variations can be reduced remarkably by appropriate selection and combination of prechamber geometry and operating parameters.

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Locuson, Charles, Mayank Patel, Akihiro Ohashi, Kenichi Iwai, Tadahiro Nambu, Toshiyuki Takeuchi, Akifumi Kogame, et al. "Abstract 5041: Translational pharmacokinetic-pharmacodynamic xenograft model for TAK-931, a small molecule cell division cycle 7 (CDC7) kinase inhibitor." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5041.

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Reports on the topic "Cell division. Cell cycle"

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Christenson, Erleen. Effect of copper on cell division, nitrogen metabolism, morphology, and sexual reproduction in the life cycle of Closterium moniliferum (Chlorophyceae). Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.54.

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Dovichi, Norman J. The Single Cell Proteome Project - Cell-Cycle Dependent Protein Expression in Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada433000.

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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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Jacobs, T. W. Regulation of cell division in higher plants. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/5089653.

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Zerbini, Luiz F. Cell Cycle Target-based Therapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada493717.

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Zarbini, Luiz. Cell Cycle Target-Based Therapy of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada485055.

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Zhan, Qimin. Gadd45 Mediates the BRCA1-Induced Cell Cycle Arrest. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada396976.

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MAISH, ALEXANDER B., ERIC J. NILAN, and PAUL M. BACA. Characterization of Fuel Cell Vehicle Duty Cycle Elements. Office of Scientific and Technical Information (OSTI), December 2002. http://dx.doi.org/10.2172/808604.

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