Relevant bibliographies by topics / Cells

Academic literature on the topic 'Cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Cells"

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Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.
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MG, Bottone. "A Brief Communication on a Cell Line of Neural Stem Cells B50 Cells Treated With a New Cisplatin - Based Drug." Journal of Embryology & Stem Cell Research 2, no. 1 (2018): 1–4. http://dx.doi.org/10.23880/jes-16000108.

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Gaddikeri1, Kavitha, and Deepak D. Bhorgonde2. "Assessment of role of mast cells in oral squamous cell carcinoma." Asian Pacific Journal of Health Sciences 3, Supplimentary 2016 (December 31, 2016): 63–66. http://dx.doi.org/10.21276/apjhs.2016.3.4s.9.

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Abramova, V. A., A. Kali, N. Abdolla, O. Yu Yurikova, Yu V. Perfilyeva, Ye O. Ostapchuk, R. T. Tleulieva, S. K. Madenova, and N. N. Belyaev. "Influence of tumor cells on natural killer cell phenotype and cytotoxicity." International Journal of Biology and Chemistry 8, no. 1 (2015): 9–14. http://dx.doi.org/10.26577/2218-7979-2015-8-1-9-14.

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CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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YAMAMOTO, Takamitsu. "C207 DEVELOPMENT OF FUEL CELLS POWERED RAILWAY VEHICLE(Fuel Cell-1)." Proceedings of the International Conference on Power Engineering (ICOPE) 2009.2 (2009): _2–213_—_2–218_. http://dx.doi.org/10.1299/jsmeicope.2009.2._2-213_.

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Ahmed Elkammar, Hala. "Effect of human bone marrow derived mesenchymal stem cells on squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 110–16. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.14.

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.
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J, Otsuka. "A Theoretical Study on the Cell Differentiation Forming Stem Cells in Higher Animals." Physical Science & Biophysics Journal 5, no. 2 (2021): 1–10. http://dx.doi.org/10.23880/psbj-16000191.

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The recent genome sequencing of multicellular diploid eukaryotes reveals an enlarged repertoire of protein genes for signal transmission but it is still difficult to elucidate the network of signal transmission to drive the life cycle of such an eukaryote only from biochemical and genetic studies. In the present paper, a theoretical study is carried out for the cell differentiation, the formation of stem cells and the growth from a child to the adult in the higher animal. With the intercellular and intracellular signal transmission in mind, the cell differentiation is theoretically derived from the process by the transition of proliferated cells from proliferation mode to differentiation mode and by both the long-range interaction between distinctive types of cells and the short-range interaction between the same types of cells. As the hierarchy of cell differentiation is advanced, the original types of self-reproducible cells are replaced by the self-reproducible cells returned from the cells differentiated already. The latter type of self-reproducible cells are marked with the signal specific to the preceding differentiation and become the stem cells for the next stage of cell differentiation. This situation is realized under the condition that the differentiation of cells occurs immediately after their proliferation in the development. The presence of stem cells in the respective lineages of differentiated cells strongly suggests another signal transmission for the growth of a child to a definite size of adult that the proliferation of stem cells in one lineage is activated by the signal from the differentiated cells in the other lineage(s) and is suppressed by the signal from the differentiated cells in its own lineage. This style of signal transmission also explains the metamorphosis and maturation of germ cells in higher animals.
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Fujimoto, Naohiro, Bin Han, Masayoshi Nomura, and Tetsuro Matsumoto. "WS1-1-1 Nitrogen-Containing Bisphosphonates Inhibit the Growth of Renal Cell Carcinoma Cells(Renal Cell Cancer)." Japanese Journal of Urology 99, no. 2 (2008): 142. http://dx.doi.org/10.5980/jpnjurol.99.142_1.

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Dissertations / Theses on the topic "Cells"

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Islam, Azharul. "Cell-walls of growing plant cells." Thesis, University of Westminster, 2013. https://westminsterresearch.westminster.ac.uk/item/8z033/cell-walls-of-growing-plant-cells.

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The plant primary cell wall is a three-dimensional interwoven network of cellulose microfibrils, cross-linked by xyloglucan and dispersed in a pectin matrix. It has been suggested that in the wall of growing plant cells, xyloglucan is bound to the rigid cellulose microfibrils by hydrogen bonds and holds the microfibrils together by forming molecular tethers, which is referred to as the ‘sticky network’ model. Plant growth occurs when these tethers are peeled from the microfibrils by expansins or broken by glycosidases or transglycosylases. A number of researchers have presented theoretical difficulties and observations inconsistent with this model and a new hypothesis has been proposed, claiming that the cellulose – xyloglucan cross-links may act as ‘scaffolds’ holding the microfibrils apart. Analogies with synthetic polymers suggests that the spacing between the cellulose microfibrils may be an important determinant of the mechanical properties of the cell wall and the results presented in this thesis support this hypothesis. Water contents of Acetobacter xylinus synthesized cellulose based cell wall analogues (as a mimic of primary cell wall) and sunflower hypocotyl cell walls were altered using high molecular weight polyethylene glycol (PEG) solution, and their extension under a constant load was measured using a creep extensiometer and showed that there were clear reduction (30-35%) in extensibility suggesting that water content of the wall and therefore the cell wall free volume directly influence wall extensibility. When hydration of A. xylinus cellulose composite pellicles was reduced using PEG 6000 solution and re-hydrated in buffer solution, followed by treatment with α-expansin or snail acetone powder extract, it was found that expansin and snail powder extracts caused a rapid rehydration of the composites and that the pellicles only returned to their original weights after these treatments, suggesting that expansin and snail powder can increase the free volume of the wall perhaps contributing to the increases in extensibility that they cause. Assays on cell wall fragments also indicated that expansin increased the cell wall free volume, demonstrated by changes of the turbidity of fragment suspensions. The role of pectic polysaccharide, RG-II, in cell wall biomechanics was also investigated using mechanical and biochemical testing of available Arabidopsis thaliana cell wall mutants and by incorporating RG-II (purified from red wine) with Acetobacter cellulose. It was demonstrated that RG-II significantly increased the hydration of cellulose composite; hydration rate was 15 -16% more than the composite without RG-II and thus increased the pellicle extensibility. From the results, it is evidenced that cell wall extension is not only the consequences of breaking hydrogen bonds between cellulose microfibrils and xyloglucan by expansins or glycosidases and transglycosylases, but also a wider range of factors are involved including cell wall water content, cell wall free volume and the pectic polymers, especially RG-II.
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Koreeda, Satoshi. "Basal cell carcinoma cells resemble follicular matrix cells rather than follicular bulge cells." Kyoto University, 2004. http://hdl.handle.net/2433/147556.

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Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.

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Carnathan, Diane Gail Vilen Barbara J. "Dendritic cell regulation of B cells." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1200.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Microbiology and Immunology, School of Medicine." Discipline: Microbiology and Immunology; Department/School: Medicine.
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Iqbal, Syed Amir. "Asymmetric Cell Division in Mammalian Cells." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503635.

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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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BARBERI, CHIARA. "Myeloma cells induce the accumulation of activated CD94low NK cells by cell-to-cell contacts involving CD56 molecules." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/996094.

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Natural Killer (NK) cells represent innate effector cells potentially able to play a role during the immune response against Multiple Myeloma (MM). To better define the distribution and the specific properties of NK cell subsets during MM disease, we analyzed their features in the bone marrow and peripheral blood of newly diagnosed MM patients. Our findings revealed that, in both compartments, NK cells were more abundant than in healthy donors. Among total MM-NK cells, a significant increase of CD94lowCD56dim NK cell subset was observed, which already appears in clinical precursor conditions leading to MM, namely monoclonal gammopathy of undetermined significance and smoldering MM, and eventually accumulates with disease progression. Moreover, a consistent fraction of CD94lowCD56dim NK cells was in a proliferation phase. When analyzed for their killing abilities, they represented the main cytotoxic NK cell subset against autologous MM cells. In vitro, MM cells could rapidly induce the expansion of the CD94lowCD56dim NK cells subset, thus reminiscent of that observed in MM patients. Mechanistically, this accumulation relied on cell to cell contacts between MM and NK cells and required both activation via DNAM-1 and homophilic interaction with CD56 expressed on MM cells. Considering the growing variety of combination treatments aimed at enhancing NK cell-mediated cytotoxicity against MM, these results may also be informative for optimizing current immunotherapeutic approaches.
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Liu, Hao. "Dendritic cell development directed by stromal cells." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516409.

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Crawford, A. "How B cells influence T cell responses." Thesis, University of Edinburgh, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.645118.

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Although studies using B cell deficient mice have been useful in understanding the importance of B cells under different conditions, it is difficult to then dissect exactly how B cells could be regulating T cell responses. By transferring OT-II transgenic T cells into either B cell deficient (μMT) or C57BL/6 mice, expansion and contraction of T cells can be tracked ex vivo. Expansion of OT-II cells is reduced in μMT mice compared to C57BL/6 mice. Thus, B cells can provide costimulatory signals, secrete cytokines and influence the lymphoid microarchitecture. To dissect which B cell factor(s) are involved in enhancing OT-II T cell expansion, a model system was used where one molecule on the B cells is depleted at one time. This was achieved by creating bone-marrow chimeras using a combination of μMT bone-marrow and wildtype or deficient bone-marrow. Thus, all the B cells are either wildtype or deficient for a particular molecule. The molecules examined were MHC-II, which is required for antigen presentation, CD40, due to its costimulatory role, and lymphotoxin-alpha, for its role in maintenance of splenic architecture. Using the OT-II adoptive transfer system, we have shown a requirement for MHC-II but not CD40 on B cells for efficient T cell expansion. In light of these observations, the role of B cell-derived MHC-II for T cell memory generation was examined. To do this, I used MHC-II tetramers to track a polyclonal population of T cells in the host.  Using this technique, I have shown that T cell memory is also diminished when the B cells do not express MHC-II. Thus, a cognate interaction with B cells is required for both efficient expansion and memory generation of CD4+ T cells.
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El-Sherbiny, Yasser Mohamed. "Natural killer cells and plasma cell neoplasia." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438481.

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Books on the topic "Cells"

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Ballard, Carol. Cells and cell function. New York: Rosen Central, 2010.

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Ltd, Addison-Wesley Longman, and Pearson Education Canada Inc, eds. Cells and cell systems. Toronto, Ont: Addison-Wesley, 2000.

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Bernard, A., B. Griffiths, W. Noé, and F. Wurm, eds. Animal Cell Technology: Products from Cells, Cells as Products. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/0-306-46875-1.

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Katin, P. Cells, cells, and more cells. Moscow: Raduga, 1990.

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Al-Rubeai, Mohamed, and Mariam Naciri, eds. Stem Cells and Cell Therapy. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7196-3.

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Irina, Klimanskaya, and Lanza Robert, eds. Adult stem cells. Amsterdam: Elsevier Academic Press, 2006.

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Ayane, Hitomi, and Katoaka Masuyo, eds. Daughter cells: Properties, characteristics, and stem cells. Hauppauge, N.Y: Nova Science Publishers, 2009.

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W, Masters J. R., Palsson Bernhard, and Thomson James A. Dr, eds. Embryonic stem cells. Dordrecht: Springer, 2007.

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Irina, Klimanskaya, and Lanza Robert, eds. Embryonic stem cells. Amsterdam: Elsevier Academic Press, 2006.

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R, Koller Manfred, Palsson Bernhard, and Masters J. R. W, eds. Primary hematopoietic cells. Dordrecht: Kluwer Academic Publishers, 1999.

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Book chapters on the topic "Cells"

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Kriegler, Michael. "Cells and Cell Lines." In Gene Transfer and Expression, 85–95. London: Palgrave Macmillan UK, 1990. http://dx.doi.org/10.1007/978-1-349-11891-5_4.

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Edelstein-Keshet, Leah. "Pattern Formation Inside Living Cells." In SEMA SIMAI Springer Series, 79–95. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-86236-7_5.

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AbstractWhile most of our tissues appear static, in fact, cell motion comprises an important facet of all life forms, whether in single or multicellular organisms. Amoeboid cells navigate their environment seeking nutrients, whereas collectively, streams of cells move past and through evolving tissue in the development of complex organisms. Cell motion is powered by dynamic changes in the structural proteins (actin) that make up the cytoskeleton, and regulated by a circuit of signaling proteins (GTPases) that control the cytoskeleton growth, disassembly, and active contraction. Interesting mathematical questions we have explored include (1) How do GTPases spontaneously redistribute inside a cell? How does this determine the emergent polarization and directed motion of a cell? (2) How does feedback between actin and these regulatory proteins create dynamic spatial patterns (such as waves) in the cell? (3) How do properties of single cells scale up to cell populations and multicellular tissues given interactions (adhesive, mechanical) between cells? Here I survey mathematical models studied in my group to address such questions. We use reaction-diffusion systems to model GTPase spatiotemporal phenomena in both detailed and toy models (for analytic clarity). We simulate single and multiple cells to visualize model predictions and study emergent patterns of behavior. Finally, we work with experimental biologists to address data-driven questions about specific cell types and conditions.
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Koido, Shigeo, and Jianlin Gong. "Cell Fusion Between Dendritic Cells and Whole Tumor Cells." In Methods in Molecular Biology, 185–91. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2703-6_13.

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Balkan, Naci, and Ayşe Erol. "Solar Cells (Photovoltaic Cells)." In Graduate Texts in Physics, 157–92. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-44936-4_5.

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Feeback, Daniel L. "Cells." In Oklahoma Notes, 1–27. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4630-5_1.

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Van Lommel, Alfons T. L. "Cells." In From Cells to Organs, 9–58. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0353-8_3.

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Yan, Lizhi, Lixin Wang, Yulan Geng, Ke Cao, Yu Cao, Yang Gao, Hui Zhang, et al. "Cells." In Urine Formed Elements, 25–74. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-7739-0_2.

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Mannerström, Bettina, Sippy Kaur, and Riitta Seppänen-Kaijansinkko. "Cells." In Tissue Engineering in Oral and Maxillofacial Surgery, 27–33. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24517-7_3.

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Dye, Frank J. "Cells." In Human Life Before Birth, 9–16. Second edition. | Boca Raton : Taylor & Francis, 2019.: CRC Press, 2019. http://dx.doi.org/10.1201/9781351130288-3.

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"The Roles of Tumor Endothelial Cells in Cancer Metastasis." In Metastasis. Exon Publications, 2022. http://dx.doi.org/10.36255/exon-publications.metastasis.endothelial-cells.

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Conference papers on the topic "Cells"

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Gil, Chang-Hyun, Dibyendu Chakraborty, Cristiano P. Vieira, Nutan Prasain, Sergio Li Calzi, Seth D. Fortmann, Ping Hu, et al. "Human Pluripotent Stem Cells from Diabetic and Nondiabetics Improve Retinal Pathology in Diabetic Mice." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021033.

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Best, Marianne, Debashis Sarker, and Claire M. Wells. "Exploring the Effect of PAK Inhibition in a 3D Pancreatic Cancer Invasion Model." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021032.

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Di Donato, Marzia, Pia Giovannelli, Antimo Migliaccio, and Gabriella Castoria. "New Approaches Targeting the Invasive Phenotype of Prostate Cancer-Associated Fibroblasts." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021001.

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Berardini, Marika, Luisa Gesualdi, Francesca Ferranti, Maria Addolorata Mariggiò, Caterina Morabito, Simone Guarnieri, Giulia Ricci, and Angela Catizone. "Microgravity Exposure Alterations of Cellular Junctions Proteins in TCam-2 Cells: Localization and Interaction." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021002.

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Di Donato, Marzia, Giovanni Galasso, Gustavo Cernera, Antimo Migliaccio, and Gabriella Castoria. "The Nerve-Growth Factor Signaling in Gender-Related Cancers." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021004.

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Natale, Francesca, Matteo Spinelli, Saviana Antonella Barbati, Lucia Leone, Salvatore Fusco, and Claudio Grassi. "Maternal High Fat Diet Multigenerationally Impairs Hippocampal Adult Neurogenesis." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021003.

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Safwan-Zaiter, Hasan, Kay-Dietrich Wagner, and Nicole Wagner. "The Senescence Marker p16Ink4a—A Player of Liver Endothelial Cells Physiology." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021013.

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Chowdhury, Nazela Ahmed, Fatema Akter Sadia, Ismat Jahan Anee, and Ashfaqul Muid Khandaker. "The Effect of RAS2 Gene Mutation in Single Cell Yeast Model." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021009.

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Cohen-Armon, Malka. "An Unveiled Cell Death Mechanism Exclusive to Human Cancer Cells." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021014.

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Sorrentino, Carmela, Giulia Gentile, Rosa D’Angiolo, Carmela Barra, Ferdinando De Stefano, Fabrizio Licitra, Emilia Sabbatino, et al. "The Role of the Androgen Receptor in Skeletal Muscle and Its Utility as a Target for Restoring Muscle Functions." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021005.

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Reports on the topic "Cells"

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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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Williams, Thomas, Caroline Erolin, and Muireann McMahon. Cell Survival: Deluxe Edition. University of Dundee, May 2023. http://dx.doi.org/10.20933/100001283.

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Cells are the smallest units of life. The environment around cells is always changing and cells need to adapt to survive. Can you keep your cell alive in this special edition of Cell Survival? Great for 1 or more people age 3+, lasts around 15 mins per game.
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Williams, Thomas. Cell Biology Board Game: Cell Survival (School Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001270.

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Cells are the smallest units of life. The environment around cells is always changing. Cells need to adapt to survive. This curriculum linked game and lesson plan introduces the world of cells to pupils 8-13. But can they keep their cells alive? This is a guide to how the cell survival resources can be used in a lesson and can be adapted as the teacher sees fit to do so. This lesson is aimed at 8-13 year olds, and fits into an hour long session. The Cell Survival Game has been adapted for both home use and for use in the classroom, and is accompanied by a series of videos. Learning Outcomes – Cells are the smallest unit of life – There are many different types of cells, and some examples of cell types – Cells experience many dangers, and some examples of dangers – How cells notice and defend themselves against dangers Links to the Curriculum – Health and Wellbeing: I am developing my understanding of the human body – Languages: I can find specific information in a straight forward text (book and instructions) to learn new things, I discover new words and phrases (relating to cells) – Mathematics: I am developing a sense of size and amount (by using the dice), I am exploring number processes (addition and subtraction) and understand they represent quantities (steps to finish line), I am learning about measurements (cell sizes) and am exploring patterns (of cell defences against dangers) – Science: I am learning about biodiversity (different types of microbes), body systems, cells and how they work. – Technology: I am learning about new technologies (used to understand how cells work).
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Williams, Thomas. Cell Biology Board Game: Cell Survival (Home Version). University of Dundee, 2022. http://dx.doi.org/10.20933/100001271.

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Williams, Thomas, Caroline Erolin, and Muireann McMahon. Cell Survival Deluxe: School Version. University of Dundee, July 2023. http://dx.doi.org/10.20933/100001284.

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Cells are the smallest units of life. The environment around cells is always changing. Cells need to adapt to survive. This curriculum linked game and lesson plan introduces the world of cells to pupils 8-13. But can they keep their cells alive? This is a guide to how the cell survival resources can be used in a lesson and can be adapted as the teacher sees fit to do so. This lesson is aimed at 8-13 year olds, and fits into an hour long session. This Cell Survival Game has been adapted for use in the classroom and contains new and improved artwork. Accompanying videos and activity sheets complete the learning experience. Learning Outcomes – Cells are the smallest unit of life – There are many different types of cells, and some examples of cell types – Cells experience many dangers, and some examples of dangers – How cells notice and defend themselves against dangers Links to the Curriculum – Health and Wellbeing: I am developing my understanding of the human body – Languages: I can find specific information in a straight forward text (book and instructions) to learn new things, I discover new words and phrases (relating to cells) – Mathematics: I am developing a sense of size and amount (by using the dice), I am exploring number processes (addition and subtraction) and understand they represent quantities (steps to finish line), I am learning about measurements (cell sizes) and am exploring patterns (of cell defences against dangers) – Science: I am learning about biodiversity (different types of microbes), body systems, cells and how they work. – Technology: I am learning about new technologies (used to understand how cells work). Accompanying videos and activity sheets (available at https://dx.doi.org/10.20933/100001270) complete the learning experience.
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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada415526.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells With a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423810.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada476353.

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Jones, Jonathan. Cell-Matrix Interactions in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300395.

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Lopez, C. M., X. Yao, R. Samajdar, and K. Vajaria. Assembling coin cells in half cell format. National Physical Laboratory, April 2024. http://dx.doi.org/10.47120/npl.mgpg153.

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