Готові списки джерел за темами / Cells Growth

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Добірка наукової літератури з теми "Cells Growth"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 28 січня 2023

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Статті в журналах з теми "Cells Growth"

1

PD, Gupta. "Liver Cells Can Dedifferentiate and Act as Progenitor Cells for Liver Growth." Journal of Embryology & Stem Cell Research 3, no. 2 (2019): 1–2. http://dx.doi.org/10.23880/jes-16000124.

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2

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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3

LIU, LINTAO, SACHIKO ITO, NAOMI NISHIO, YANG SUN, YURIKO TANAKA, and KEN-ICHI ISOBE. "GADD34 Promotes Tumor Growth by Inducing Myeloid-derived Suppressor Cells." Anticancer Research 36, no. 9 (September 9, 2016): 4623–28. http://dx.doi.org/10.21873/anticanres.11012.

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4

Nagamalleswari, D., and Y. B. Kishore Kumar. "Growth of Cu2ZnSnS4 Thin Film Solar Cells Using Chemical Synthesis." Indian Journal Of Science And Technology 15, no. 28 (July 28, 2022): 1399–405. http://dx.doi.org/10.17485/ijst/v15i28.194.

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5

Balch, Ying. "Subculture human skeletal muscle cells to produce the cells with different Culture medium compositions." Clinical Research and Clinical Trials 3, no. 4 (April 30, 2021): 01–03. http://dx.doi.org/10.31579/2693-4779/036.

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This study aimed to subculture human skeletal muscle cells (HSkMC) using a culture medium with different compositions to determine the most efficient medium for the growth of the human skeletal muscle cells. The culture media was divided into three groups: Group1. An HSkMC growth medium. Group 2. An HSkMC growth medium + with 10% high glucose (GH). Group 3. An HSkMC growth medium + 10% fetal bovine serum (FBS). HSkMC from groups 1 to 3 gradually became round in shape and gathered in clusters. These changes differed between the groups. In group 3, the HSkMC clusters were more in numbers and gathered as significantly more prominent than in the other groups under the EVOS-Microscope shown. We concluded that by manipulating the composition of the culture medium, it is possible to induce HSkMC to promote the best growth.
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6

González-Quirós, Rafael, Iyziar Munuera, and Arild Folkvord. "Cell cycle analysis of brain cells as a growth index in larval cod at different feeding conditions and temperatures." Scientia Marina 71, no. 3 (July 30, 2007): 485–97. http://dx.doi.org/10.3989/scimar.2007.71n3485.

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7

Brombin, Chiara, Massimo Crippa, and Clelia Di Serio. "Modeling Cancer Cells Growth." Communications in Statistics - Theory and Methods 41, no. 16-17 (August 2012): 3043–59. http://dx.doi.org/10.1080/03610926.2012.685547.

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8

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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9

Gärtner, Roland, Petra Rank та Birgit Ander. "The role of iodine and δ-iodolactone in growth and apoptosis of malignant thyroid epithelial cells and breast cancer cells". HORMONES 9, № 1 (15 січня 2010): 60–66. http://dx.doi.org/10.14310/horm.2002.1254.

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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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Анотація:
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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Дисертації з теми "Cells Growth"

1

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

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2

Stocking, Carol E. "Autonomous growth of haematopoietic cells." Thesis, Brunel University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.290956.

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3

Greene, Elizabeth Ann 1964. "The effects of growth factors on bovine satellite cells." Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277202.

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This study examined the effects of basic fibroblast growth factor (bFGF), insulin-like growth factor I (IGF-I) and transforming growth factor beta (TGF-β) on the proliferation and differentiation of bovine satellite cells (BSC) in vitro. Cells were treated with serum-free defined media containing varying concentrations of bFGF, IGF-I and TGF-β. On day 3 of treatment total cell nuclei and myotube nuclei were determined. bFGF stimulated BSC proliferation in a dose-dependent fashion with half-maximal stimulation observed at a concentration of 5 ng/ml (p < .05). Similar results were found for IGF-I and TGF-β in the presence of FGF, with half-maximal stimulation observed at 5 ng/ml and 1 ng/ml, respectively. With regard to differentiation, TGF-beta inhibited myotube formation at concentrations above 0.05 ng/ml. IGF-I stimulated myotube formation at concentrations as low as 10 ng/ml (p < .05). These results demonstrate that proliferation and differentiation of BSC in vitro are affected by growth factors, and consequently, similar effects may be found in vivo. This information may prove to be useful in future methods of manipulating muscle growth in vivo.
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4

Li, Jing. "Effects of intrinsic & extrinsic factors on the growth and differentiation of human mesenchymal stem cells." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36434450.

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5

Hou, Yuen-chi Denise, and 侯元琪. "A comparative study on the effects of feeder cells on culture of human embryonic stem cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hdl.handle.net/10722/210317.

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6

McGuiness, Lindsay. "Transgenes targeted to growth hormone cells." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405167.

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7

Anilkumar, Thapasimuthu Vijayamma. "The pathobiology of hepatic stem cells (oval cells)." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244072.

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8

Barry, Megan M. Crockett Robert S. "Three-dimensional scaffolds for mammary epithelial cell growth : a thesis /." [San Luis Obispo, Calif. : California Polytechnic State University], 2008. http://digitalcommons.calpoly.edu/theses/12/.

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Анотація:
Thesis (M.S.)--California Polytechnic State University, 2008.
Major professor: Robert S. Crockett, Ph.D. "Presented to the faculty of California Polytechnic State University, San Luis Obispo." "In partial fulfillment of the requirements for the degree [of] Master of Science in Engineering." "May 2008." Includes bibliographical references (leaves 38-45). Also available on microfiche (1 sheet).
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9

Johansson, Magnus. "Role of Islet Endothelial Cells in β-cell Function and Growth". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6801.

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Анотація:
The pancreatic islets are collections of endocrine cells, dispersed throughout the pancreas. In adult islets, endocrine cells are closely associated with capillary endothelial cells and receive a high blood perfusion. Transplanted pancreatic islets, on the other hand, have a vascular disturbance, manifested as decreased blood vessel density. Besides impaired islet blood perfusion and oxygenation, this means that the normal close proximity between endothelial cells and β-cell in adult islets is interrupted. The aim of the thesis was to investigate if, and to what extent, β-cells and islet endothelial cells can interact with one another. This hypothesis was investigated during physiological growth of pancreatic islets, following transplantation and in vitro. We observed that islet endothelial and endocrine cell replication coincided immediately after birth, as well as during pregnancy. In pregnant animals, β-cell proliferation colocalized to islets with increased endothelial cell replication, indicating that the two processes were interconnected. The pregnancy hormone prolactin favored endothelial cell replication, and these activated cells could then augment β-cell proliferation. We found that prolactin pretreatment increased blood vessel density and oxygen tension in islets after transplantation. Furthermore, prolactin pretreatment improved endocrine function in a minimal islet transplant model. Partial pancreatectomy performed in association with islet transplantation improved revascularization, oxygen tension and glucose stimulated insulin release from the graft. In conclusion, the findings suggest that endocrine and endothelial cells interact with one another to regulate growth and function in pancreatic islets. This may form the basis for interventions aiming to improve revascularization and function of transplanted islets.
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10

Mittal, Nikhil 1979. "Cell-cell and cell-medium interactions in the growth of mouse embryonic stem cells." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/62602.

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Анотація:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Physics, 2010.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (p. 100-108).
Embryonic stem cells serve as powerful models for the study of development and disease and hold enormous potential for future therapeutics. Due to the potential for embryonic stem cells (ESCs) to provide a variety of tissues for use in regenerative medicine, there has been great interest in the identification of factors that govern the differentiation of ESCs into specific lineages. Much of this research builds on previous studies of the role of intercellular signaling in the specification of various cell types in the developing embryo. However, relatively little work has been done on understanding the role of cell-cell communication in the self-renewal of ESCs. In the first part of this thesis I describe the development and testing of new devices for studying intercellular signaling - the nDEP microwell array and the Bio Flip Chip (BFC). We used the BFC to show that cell-cell interaction improves the colony-forming efficiency and the self-renewal of mouse ESCs. Further, we demonstrate that the interaction is at least partly diffusible. In the next part of the thesis I describe our use of more traditional assays to validate the results obtained using the BFC and to further explore the role of diffusible signaling in the survival of mouse ESCs. We demonstrate the existence of an optimal density for 2-day culture of mouse ESCs. Further, we demonstrate that the increase in growth with plating density (103-104 cells/cm2) is at least partly due to the existence of one or more survival-enhancing autocrine factor(s) in mouse ESC cultures, and that one of these factors is Cyclophilin A. Finally, we demonstrate that changes in the low molecular weight composition of the medium are likely responsible for the decrease in growth at high plating densities (>104 cells/cm2). We use a numerical model to show that competition between the positive effect (on growth) of autocrine survival factors and the negative effect of nutrient depletion can account for the observed optimal growth density. Our study provides new insight into the processes underlying, and optimization of, growth in cell types that lack contact inhibition such as cancer cells and stem cells.
by Nikhil V. Mittal.
Ph.D.
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Книги з теми "Cells Growth"

1

Takumi, Hayashi, ed. Progress in cell growth process research. New York: Nova Science Publishers, 2008.

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2

Stocking, Carol E. Autonomous growth of haematopoietic cells. Uxbridge: Brunel University, 1989.

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3

M, Shapiro Irving, Boyan Barbara, and Anderson H. Clarke, eds. The growth plate. Amsterdam: IOS Press, 2002.

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4

Kulkarni, Rohit N. Islet cell growth factors. Austin, Tex: Landes Bioscience, 2011.

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5

A, Bryant J., and Chiatante Donato, eds. Plant cell proliferation and its regulation in growth and development. Chichester: Wiley, 1998.

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6

Ou, Che-wei. Regulation of cell-cell communication and growth in normal and neoplastic cells. Ottawa: National Library of Canada, 1994.

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7

Stem cell biology in health and disease. Dordrecht: Springer, 2009.

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8

Nakajima, K., and Noritaka Usami. Crystal growth of Si for solar cells. Berlin: Springer Verlag, 2009.

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9

Kaur, Maninder. Growth and differentiation of liver epithelial cells. Birmingham: University of Birmingham, 2001.

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10

M, Carlson Bruce, ed. Growth and hyperplasia of cardiac muscle cells. London, U.K: Harwood Academic Publishers, 1991.

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Частини книг з теми "Cells Growth"

1

Winwood, Paul J., and Michael J. P. Arthur. "Kupffer cells and endothelial cells." In Liver Growth and Repair, 482–511. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_19.

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2

Ankoma-Sey, Victor, and Scott L. Friedman. "Hepatic stellate cells." In Liver Growth and Repair, 512–37. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_20.

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3

Karma, Alain, and Pierre Pelcé. "Deep Cells in Directional Solidification." In Growth and Form, 147–56. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-1357-1_14.

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4

Dey, S. K., B. C. Paria, S. K. Das, and G. K. Andrews. "Trophoblast-Uterine Interactions in Implantation: Role of Transforming Growth Factor α/Epidermal Growth Factor Receptor Signaling." In Trophoblast Cells, 71–91. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4612-2718-2_5.

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5

Kawabe, Yoh-ichi, and Michael A. Rudnicki. "The Role of Satellite Cells and Stem Cells in Muscle Regeneration." In Handbook of Growth and Growth Monitoring in Health and Disease, 1289–304. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_77.

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6

Koch, Arthur L. "Turgor Pressure of Bacterial Cells." In Bacterial Growth and Form, 118–42. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1779-5_5.

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Koch, Arthur L. "Turgor Pressure of Bacterial Cells." In Bacterial Growth and Form, 135–60. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0827-2_6.

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8

Grout, B. W. W. "Minimal Growth Storage." In Genetic Preservation of Plant Cells in Vitro, 21–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78661-7_2.

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9

Rechler, Matthew M., Yvonne W. H. Yang, Jeffrey E. Terrell, Angela M. Acquaviva, Harvey J. Whitfield, Joyce A. Romanus, C. Bruno Bruni, and S. Peter Nissley. "Biosynthesis of Rat Insulinlike Growth Factor II in Intact Cells and Cell-Free Translation." In Human Growth Hormone, 529–37. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_42.

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10

Brandt, Ralf, and Andreas D. Ebert. "Growth Inhibitors for Mammary Epithelial Cells." In Inhibitors of Cell Growth, 197–248. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72149-6_10.

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Тези доповідей конференцій з теми "Cells Growth"

1

Weinbaum, Sheldon. "Mechano/Transduction, Cellular Communication and Fluid Flow in Tissue Engineering." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2511.

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Abstract The growth of cellular constructs in tissue scaffolds depends on the delivery of nutrients and growth factors as well as the substrate on which they are grown. Micropatterning techniques have also made it possible to grow cells on a wide variety of substrates with greatly different topography which significantly alter cellular contact and communication. Fluid flow is critical not only in this delivery of nutrients and growth factors, but also in the interaction of the cell’s cytoskeleton with its attachment matrix. Similarly, fluid flow is known to play an important role in cell to cell communication via its regulatory effect on various gap junction proteins of the connexon family. The mechano/transduction and cell to cell signaling mechanisms will be examined for both cells with a smooth topography, such as vascular endothelium cells which are involved in angiogenesis and cells with cell processes and microvilli whose tethering attachments and protrusions interact with fluid flow in a different manner.
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2

Kanthou, C., C. Parker, D. E. Huber, P. Stroobant, V. V. Kakkar, N. Pringle, and W. Richardson. "PLATELET-DERIVED GROWTH FACTORA-CHAIN GENE ACTIVATION AND GROWTH FACTOR PRODUCTION BY HUMAN AORTIC SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643751.

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The many contributory factors leading to the development of cardiovascular disease are currently thought to induce a common pathological change involving smooth muscle cells, which migrate from the vessel wall, proliferate,accumulate at the sites of endothelial cell damage, and then secrete connective tissue proteins and lipids which contribute to the plaque which results in the occlusion of the vessel. According to the recently modified hypothesis of Ross (1), a key event in the development of atheroma may be the abnormal release of a number of growth modulatory polypeptides,including platelet-derived growth factor (PDGF), which can potentially originate from platelets, endothelial cells, monocytes or macrophages, and smooth muscle cells themselves.We have isolated smooth muscle cell lines from 25 samples of human aorta, using digestion with collagenase and elastase. With DNA synthesis and Northern blot techniques, we examined them for both the production of PDGF-like proteins, and for the possible activation of the PDGF A-chain and B-chain genes. Severallines secreted a growth factor and were stillviable after culture for 57 days in serum-free medium. Parallel experiments using Northernblot analysis revealed the activation of the PDGF A-chain gene in all lines examined with no detectable B-chain gene transcripts.These data raise the possibility that vascular damage may activate the gene encoding the A-chain of PDGF in adjacent smooth muscle cells. Such cells might then become capable ofautonomous growth, in an analogous manner tocells transformed by Simian Sarcoma Virus, whose sis oncogene encodes the B-chain of PDGF.
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3

Chambouleyron, I. "MULTIJUNCTION SOLAR CELLS." In Proceedings of the International School on Crystal Growth and Characterization of Advanced Materials. WORLD SCIENTIFIC, 1988. http://dx.doi.org/10.1142/9789814541589_0022.

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4

Li, Q., S. Demir, X. Bao, A. Wagner, Y. Fan, S. Cairo, and R. Kappler. "Mebendazole inhibits growth of hepatoblastoma cells by cell cycle arrest." In 34. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1748714.

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Chen, Kok Hao, and Jong Hyun Choi. "Nanoparticle-Aptamer: An Effective Growth Inhibitor for Human Cancer Cells." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11966.

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Semiconductor nanocrystals have unique optical properties due to quantum confinement effects, and a variety of promising approaches have been devised to interface the nanomaterials with biomolecules for bioimaging and therapeutic applications. Such bio-interface can be facilitated via a DNA template for nanoparticles as oligonucleotides can mediate the aqueous-phase nucleation and capping of semiconductor nanocrystals.[1,2] Here, we report a novel scheme of synthesizing fluorescent nanocrystal quantum dots (NQDs) using DNA aptamers and the use of this biotic/abiotic nanoparticle system for growth inhibition of MCF-7 human breast cancer cells for the first time. Particularly, we used two DNA sequences for this purpose, which have been developed as anti-cancer agents: 5-GGT GGT GGT GGT TGT GGT GGT GGT GG-3 (also called, AGRO) and 5-(GT)15-3.[3–5] This study may ultimately form the basis of unique nanoparticle-based therapeutics with the additional ability to optically report molecular recognition. Figure 1a shows the photoluminescence (PL) spectra of GT- and AGRO-passivated PbS QD that fluoresce in the near IR, centered at approximately 980 nm. A typical synthesis procedure involves rapid addition of sodium sulfide in the mixture solution of DNA and Pb acetate at a molar ratio of 2:4:1. The resulting nanocrystals are washed to remove unreacted DNA and ions by adding mixture solution of NaCl and isopropanol, followed by centrifugation. The precipitated nanocrystals are collected and re-suspended in aqueous solution by mild sonication. Optical absorption measurements reveal that approximately 90 and 77% of GT and AGRO DNA is removed after the washing process. The particle size distribution in Figure 1b suggests that the GT sequence-capped PbS particles are primarily in 3–5 nm diameter range. These nanocrystals can be easily incorporated with mammalian cells and remain highly fluorescent in sub-cellular environments. Figure 1c serially presents an optical image of a MCF-7 cell and a PL image of the AGRO-capped QD incorporated with the cell. Figure 1. (a) Normalized fluorescence spectra of PbS QD synthesized with GT and AGRO sequences, which were previously developed as anti-cancer agents. The DNA-capped QD fluoresce in the near IR centered at ∼980 nm. (b) TEM image of GT-templated nanocrystals ranging 3–5 nm in diameter. (c) Optical image of an MCF-7 human breast cancer cell after a 12-hour exposure to aptamer-capped QD. (d) PL image of AGRO-QD incorporated with the cell, indicating that these nanocrystals remain highly fluorescent in sub-cellular environments. One immediate concern for interfacing inorganic nanocrystals with cells and tissue for labeling or therapeutics is their cytotoxicity. The nanoparticle cytotoxicity is primarily determined by material composition and surface chemistry, and QD are potentially toxic by generating reactive oxygen species or by leaching heavy metal ions when decomposed.[6] We examined the toxicity of aptamer-passivated nanocrystals with NIH-3T3 mouse fibroblast cells. The cells were exposed to PbS nanocrystals for 2 days before a standard MTT assay as shown in Figure 2, where there is no apparent cytotoxicity at these doses. In contrast, Pb acetate exerts statistically significant toxicity. This observation suggests a stable surface passivation by the DNA aptamers and the absence of appreciable Pb2+ leaching. Figure 2. Viability of 3T3 mouse fibroblast cells after a 2-day exposure to DNA aptamer-capped nanocrystals. There is no apparent dose-dependent toxicity, whereas a statistically significant reduction in cell viability is observed with Pb ions. Note that Pb acetate at 133 μM is equivalent to the Pb2+ amount that was used for PbS nanocrystal synthesis at maximum concentration. Error bars are standard deviations of independent experiments. *Statistically different from control (p&lt;0.005). Finally, we examined if these cyto-compatible nanoparticle-aptamers remained therapeutically active for cancer cell growth inhibition. The MTT assay results in Figure 3a show significantly decreased growth of breast cancer cells incorporated with AGRO, GT, and the corresponding templated nanocrystals, as anticipated. In contrast, 5-(GC)15-3 and the QDs synthesized with the same sequence, which were used as negative controls along with zero-dose control cells, did not alter cell viability significantly. Here, we define the growth inhibition efficacy as (100 − cell viability) per DNA of a sample, because the DNA concentration is significantly decreased during the particle washing. The nanoparticle-aptamers demonstrate 3–4 times greater therapeutic activities compared to the corresponding aptamer drugs (Figure 3b). We speculate that when a nanoparticle-aptamer is internalized by the cancer cells, it forms an intracellular complex with nucleolin and nuclear factor-κB (NF-κB) essential modulator, thereby inhibiting NF-κB activation that would cause transcription of proliferation and anti-apoptotic genes.[7] The nanoparticle-aptamers may more effectively block the pathways for creating anti-apoptotic genes or facilitate the cellular delivery of aptamers via nanoparticle uptake. Our additional investigation indicates that the same DNA capping chemistry can be utilized to produce aptamer-mediated Fe3O4 nanocrystals, which may be potentially useful in MRI and therapeutics, considering their magnetic properties and biocompatibility. In summary, the nanoparticle-based therapeutic schemes developed here should be valuable in developing a multifunctional drug delivery and imaging agent for biological systems. Figure 3. Anti-proliferation of MCF-7 human breast cancer cells with aptamer-passivated nanocrystals. (a) Viability of MCF-7 cells exposed to AGRO and GT sequences, and AGRO-/GT-capped QD for 7 days. The DNA concentration was 10 uM, while the particles were incubated with cells at 75 nM. (b) Growth inhibition efficacy is defined as (100 − cell viability) per DNA to correct the DNA concentration after particle washing.
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6

Milad Zaltum, Mohamed A., Mohamad Nazib Adon, and Muhammad Mahadi Abdul Jamil. "Electroporation effect on growth of HeLa cells." In 2013 6th Biomedical Engineering International Conference (BMEiCON). IEEE, 2013. http://dx.doi.org/10.1109/bmeicon.2013.6687714.

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7

Wojtczuk, S., P. Chiu, X. Zhang, D. Pulver, C. Harris, B. Siskavich, Frank Dimroth, Sarah Kurtz, Gabriel Sala, and Andreas W. Bett. "42% 500X Bi-Facial Growth Concentrator Cells." In 7TH INTERNATIONAL CONFERENCE ON CONCENTRATING PHOTOVOLTAIC SYSTEMS: CPV-7. AIP, 2011. http://dx.doi.org/10.1063/1.3658283.

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8

Agriesti, F., T. Tataranni, C. Pacelli, C. Mazzoccoli, V. Ruggieri, R. Scrima, O. Cela, C. Pomara, N. Capitanio, and C. Piccoli. "PO-246 Nandrolone affects cell growth and differentiation in hepatoma cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.279.

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9

Ateshian, Gerard A., Kevin D. Costa, Evren U. Azeloglu, Barclay Morrison, and Clark T. Hung. "Continuum Modeling of Biological Tissue Growth by Cell Division." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205495.

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A framework is formulated for continuum modeling of biological tissue growth that explicitly addresses cell division, using a homogenized representation of cells and the extracellular matrix (ECM). The essential elements of this model rely on the description of the cell as containing a solution of water and osmolytes, and having osmotically inactive solid constituents that may be generically described as a porous solid matrix. The division of a cell into two nearly identical daughter cells normally starts with the duplication of cell contents during the synthesis phase, followed by cell division during the mitosis phase. Thus, ultimately, cell division is equivalent to doubling of the cell solid matrix and osmolyte content, and a resulting increase in water uptake via osmotic effects. In a homogenized representation of the tissue, the geometry of individual cells is not modeled explicitly, but their solid matrix and intracellular osmolyte content can be suitably incorporated into the analysis of the tissue response, thereby accounting for their osmotic effects. Thus, cell division can be described by the growth of these cell constituents, including the accumulation of osmotically active content, and the resultant uptake of water.
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10

Allen, Kathleen B., and Bradley E. Layton. "Mechanical Neural Growth Models." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-79445.

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Critical to being able to control the growth patterns of cell-based sensors is being able to understand how the cytoskeleton of the cell maintains its structure and integrity both under mechanical load and in a load-free environment. Our approach to a better understanding of cell growth is to use a computer simulation that incorporates the primary structures, microtubules, necessary for growth along with their observed behaviors and experimentally determined mechanical properties. Microtubules are the main compressive structural support elements for the axon of a neuron and are created via polymerization of α-β tubulin dimers. Our de novo simulation explores the mechanics of the forces between microtubules and the membrane. We hypothesize that axonal growth is most influenced by the location and direction of the force exerted by the microtubule on the membrane, and furthermore that the interplay of forces between microtubules and the inner surface of the cell membrane dictates the polar structure of axons. The simulation will be used to understand cytoskeletal mechanics for the purpose of engineering cells to be used as sensors.
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Звіти організацій з теми "Cells Growth"

1

Lau, Lester F. Growth Suppressors of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392204.

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2

Lau, Lester. Growth Suppressors of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382887.

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3

Iwamoto, Yoshiki. Cell Growth Arrest Mediated by STAT Proteins in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada358078.

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4

Borrego, J., and S. Ghandhi. Hydrogen radical enhanced growth of solar cells. Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/5307219.

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5

Furbert-Harris, Paulette. Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada394003.

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6

Olson, Daniel J. WNT-5a and WNT-4 Regulates Cell Growth in C57MG Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada299744.

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7

Olson, Daniel J. Wnt-5a and Wnt-4 Regulates Cell Growth in C57MG Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada314665.

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8

Furbert-Harris, Paulette M. Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada383068.

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9

Lin, Anning. Signaling Mechanisms of Malignant Growth of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada395744.

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10

Eisinger, Magdalena. Wound Healing by Cultured Skin Cells and Growth Factors. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada284593.

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