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Journal articles on the topic 'Cells Growth'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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

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10

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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11

Dai, Jinlu, Jacques Nor, and Evan Keller. "Human Prostate cancer cells induce osteocalcin expression in the preosteoblast MC 3T3-E1 cell line through vascular endothelial growth factor (VEGF)." Japanese Journal of Urology 96, no. 2 (2005): 154. http://dx.doi.org/10.5980/jpnjurol.96.154_4.

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12

Aversa, Raffaella, Antonio Apicella, Francesco Tamburrino, and Florian Ion Tiberiu Petrescu. "Mechanically Stimulated Osteoblast Cells Growth." American Journal of Engineering and Applied Sciences 11, no. 2 (February 1, 2018): 1023–36. http://dx.doi.org/10.3844/ajeassp.2018.1023.1036.

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13

SATO, Yasufumi. "Endothelial Cells and Growth Factors." Journal of Japan Atherosclerosis Society 21, no. 4 (1993): 329–36. http://dx.doi.org/10.5551/jat1973.21.4_329.

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14

Scheike, Thomas H. "Anisotropic Growth of Voronoi Cells." Advances in Applied Probability 26, no. 1 (March 1994): 43–53. http://dx.doi.org/10.2307/1427577.

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This paper discusses a simple extension of the classical Voronoi tessellation. Instead of using the Euclidean distance to decide the domains corresponding to the cell centers, another translation-invariant distance is used. The resulting tessellation is a scaled version of the usual Voronoi tessellation. Formulas for the mean characteristics (e.g. mean perimeter, surface and volume) of the cells are provided in the case of cell centers from a homogeneous Poisson process. The resulting tessellation is stationary and ergodic but not isotropic.
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15

Scheike, Thomas H. "Anisotropic Growth of Voronoi Cells." Advances in Applied Probability 26, no. 01 (March 1994): 43–53. http://dx.doi.org/10.1017/s0001867800025982.

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This paper discusses a simple extension of the classical Voronoi tessellation. Instead of using the Euclidean distance to decide the domains corresponding to the cell centers, another translation-invariant distance is used. The resulting tessellation is a scaled version of the usual Voronoi tessellation. Formulas for the mean characteristics (e.g. mean perimeter, surface and volume) of the cells are provided in the case of cell centers from a homogeneous Poisson process. The resulting tessellation is stationary and ergodic but not isotropic.
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16

Puro, Donald G. "Growth factors and Müller cells." Progress in Retinal and Eye Research 15, no. 1 (January 1995): 89–101. http://dx.doi.org/10.1016/1350-9462(95)00004-6.

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17

Paul, J. "Growth factors and stem cells." FEBS Letters 182, no. 1 (March 11, 1985): 211–12. http://dx.doi.org/10.1016/0014-5793(85)81192-3.

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18

Jasmin, Claude, Vassilis Georgoulias, Florence Smadja-Joffe, Claude Boucheix, Caroline Le Bousse-Kerdiles, Michèle Allouche, Christian Cibert, and Bruno Azzarone. "Autocrine growth of leukemic cells." Leukemia Research 14, no. 8 (January 1990): 689–93. http://dx.doi.org/10.1016/0145-2126(90)90095-q.

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19

Robinson, Richard. "GROWTH FACTORS AND STEM CELLS." Neurology Today 5, no. 5 (May 2005): 42. http://dx.doi.org/10.1097/00132985-200505000-00010.

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20

Luce-Fedrow, Alison, Kevin R. Macaluso, and Allen L. Richards. "Growth ofRickettsia felisinDrosophila melanogasterS2 Cells." Vector-Borne and Zoonotic Diseases 14, no. 2 (February 2014): 101–10. http://dx.doi.org/10.1089/vbz.2013.1370.

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21

Huttunen, M. "Mast cells inhibit keratinocyte growth." Journal of the European Academy of Dermatology and Venereology 5, no. 1 (October 1995): S136—S137. http://dx.doi.org/10.1016/0926-9959(95)96317-2.

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22

UNSICKER, K., and K. KRIEGLSTEIN. "Growth factors in chromaffin cells." Progress in Neurobiology 48, no. 4-5 (March 1996): 307–24. http://dx.doi.org/10.1016/0301-0082(95)00045-3.

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23

Atef Yekta, M., F. Verdonck, W. Van Den Broeck, BM Goddeeris, E. Cox, and D. Vanroy. "Lactoferrin inhibits E. coli O157:H7 growth and attachment to intestinal epithelial cells." Veterinární Medicína 55, No. 8 (September 15, 2010): 359–68. http://dx.doi.org/10.17221/2954-vetmed.

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Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 strains are associated with haemorraghic colitis and haemolytic uremic syndrome (HUS) in humans. Cattle are a reservoir of E. coli O157:H7. We studied the ability of bovine and human lactoferrin, two natural antimicrobial proteins present in milk, to inhibit E. coli O157:H7 growth and attachment to a human epithelial colorectal adenocarcinoma cell line (Caco-2). The direct antibacterial effect of bLF on E. coli O157:H7 was stronger than that of hLF. Nevertheless, both lactoferrins had bacteriostatic effects even at high concentrations (10 mg/ml), suggesting blocking of LF activity by a yet undefined bacterial defence mechanism. Additionally, both lactoferrins significantly inhibited E. coli O157:H7 attachment to Caco-2 cells. However, hLF was more effective than bLF, probably due to more efficient binding of bLF to intelectin present on human enterocytes leading to uptake and thus removal of bLF from the extracellular environment. Inhibition of bacterial attachment to Caco-2 cells was at least partly due to the catalytic effect of lactoferrins on the type III secreted proteins EspA and EspB
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24

Taetle, R. "Anti-epidermal growth factor and growth of human cells." Biomedicine & Pharmacotherapy 43, no. 6 (January 1989): 459. http://dx.doi.org/10.1016/0753-3322(89)90255-2.

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25

Schop, Deborah, Frank W. Janssen, Linda D. S. van Rijn, Hugo Fernandes, Rolf M. Bloem, Joost D. de Bruijn, and Riemke van Dijkhuizen-Radersma. "Growth, Metabolism, and Growth Inhibitors of Mesenchymal Stem Cells." Tissue Engineering Part A 15, no. 8 (August 2009): 1877–86. http://dx.doi.org/10.1089/ten.tea.2008.0345.

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26

Shiota, G., D. B. Rhoads, T. C. Wang, T. Nakamura, and E. V. Schmidt. "Hepatocyte growth factor inhibits growth of hepatocellular carcinoma cells." Proceedings of the National Academy of Sciences 89, no. 1 (January 1, 1992): 373–77. http://dx.doi.org/10.1073/pnas.89.1.373.

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27

Mizuno, K., O. Higuchi, J. N. Ihle, and T. Nakamura. "Hepatocyte Growth Factor Stimulates Growth of Hematopoietic Progenitor Cells." Biochemical and Biophysical Research Communications 194, no. 1 (July 1993): 178–86. http://dx.doi.org/10.1006/bbrc.1993.1801.

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28

Moiseev, Ivan S., Sergej V. Lapin, Elena A. Surkova, Margarita Y. Lerner, Elena V. Babenko, Alexandra A. Sipol, Vladimir N. Vavilov, and Boris V. Afanasyev. "Prognostic significance of vascular endothelial growth factor and circulating endothelial cells for early and late outcomes of allogeneic hematopoietic stem cell transplantation." Cellular Therapy and Transplantation 4, no. 1-2 (2015): 38–46. http://dx.doi.org/10.18620/1866-8836-2015-4-1-2-38-46.

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29

Bilyuk, A. A. "PT (II) AND PD (II) COMPLEXES INFLUENCE ON SPHEROIDS GROWTH OF BREAST CANCER CELLS." Biotechnologia Acta 10, no. 1 (February 2017): 61–67. http://dx.doi.org/10.15407/biotech10.01.061.

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30

L, Mazini. "Growth Differentiation Factor 11 (GDF11)/Transforming Growth Factor - β (TGF - β)/Mesenchymal Stem Cells (MSCs) Balance: A Complicated Partnership in Skin Rejuvenation." Journal of Embryology & Stem Cell Research 3, no. 2 (2019): 1–10. http://dx.doi.org/10.23880/jes-16000122.

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31

Kalluri, Haviryaji S. G., and Robert J. Dempsey. "Growth factors, stem cells, and stroke." Neurosurgical Focus 24, no. 3-4 (March 2008): E14. http://dx.doi.org/10.3171/foc/2008/24/3-4/e13.

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✓ Postischemic neurogenesis has been identified as a compensatory mechanism to repair the damaged brain after stroke. Several factors are released by the ischemic tissue that are responsible for proliferation, differentiation, and migration of neural stem cells. An understanding of their roles may allow future therapies based on treatment with such factors. Although damaged cells release a variety of factors, some of them are stimulatory whereas some are inhibitory for neurogenesis. It is interesting to note that factors like insulin-like growth factor–I can induce proliferation in the presence of fibroblast growth factor–2 (FGF-2), and promote differentiation in the absence of FGF-2. Meanwhile, factors like transforming growth factor–β can induce the differentiation of neurons while inhibiting the proliferation of neural stem cells. Therefore, understanding the role of each factor in the process of neurogenesis will help physicians to enhance the endogenous response and improve the clinical outcome after stroke. In this article the authors discuss the role of growth factors and stem cells following stroke.
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32

Sawada, Ken-Ichi. "Growth Characteristics of Myelodysplastic CD34+Cells." Leukemia & Lymphoma 29, no. 1-2 (January 1998): 49–60. http://dx.doi.org/10.3109/10428199809058381.

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33

Visani, G., R. M. Lemoli, P. Tosi, A. Dinota, C. Tassi, M. Fogli, and M. Cavo. "In vitro growth of myeloma cells*." European Journal of Haematology 43, S51 (April 24, 2009): 43–46. http://dx.doi.org/10.1111/j.1600-0609.1989.tb01491.x.

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34

Barnes, D. "Cells without growth factors commit suicide." Science 242, no. 4885 (December 16, 1988): 1510–11. http://dx.doi.org/10.1126/science.3201239.

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35

Hays, E. F., S. Kitada, C. H. Uittenbogaart, and J. R. Reeve. "Autocrine Growth of Murine Lymphoma Cells." JNCI Journal of the National Cancer Institute 80, no. 2 (March 16, 1988): 116–21. http://dx.doi.org/10.1093/jnci/80.2.116.

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36

KARALIS, T. K., KONSTANTINOS T. KARALIS, and KONSTANTINA N. PAPAVASILEIOY. "GROWTH OF MALIGNANT CELLS AND THERMODYNAMICS." Journal of Mechanics in Medicine and Biology 16, no. 02 (March 2016): 1650006. http://dx.doi.org/10.1142/s0219519416500068.

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In the present paper, certain thermodynamic relations are considered to study tumor growth and how the mechanisms, responsible for the cell killing by temperature change in abnormal cells, can be estimated from direct measurements, during evolution of a tumor. The problem is considered in its most general form and the discussion focuses on how significant results can be estimated from: (i) The stress system acting on the tumor, tumor pressure and tumor volume changes measured by ultra-sonic computerized tomography, (ii) entropy change and entropy production, measured from the heat capacity profiles, and (iii) the chemical potential changes measured by fluorescent labeling techniques; all of them supported by other techniques based on histo-chemical and microscopic methods.
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37

Rosengart, Todd K., Edgar G. Chedrawy, Gerald Patejunas, and Mauricio Retuarto. "Vascular endothelial growth factor before cells." Journal of Thoracic and Cardiovascular Surgery 129, no. 3 (March 2005): 696. http://dx.doi.org/10.1016/j.jtcvs.2004.11.018.

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38

Fraldi, Massimiliano, and Angelo R. Carotenuto. "Cells competition in tumor growth poroelasticity." Journal of the Mechanics and Physics of Solids 112 (March 2018): 345–67. http://dx.doi.org/10.1016/j.jmps.2017.12.015.

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39

Veiby, Ole P., Adel A. Mikhail, and H. Ralph Snodgrass. "GROWTH FACTORS AND HEMATOPOIETIC STEM CELLS." Hematology/Oncology Clinics of North America 11, no. 6 (December 1997): 1173–84. http://dx.doi.org/10.1016/s0889-8588(05)70487-1.

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40

Bump, Nancy J., and Victor A. Najjar. "Tuftsin stimulates growth of HL60 cells." FEBS Letters 226, no. 2 (January 4, 1988): 303–6. http://dx.doi.org/10.1016/0014-5793(88)81444-3.

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41

Jorgensen, Paul, and Mike Tyers. "How Cells Coordinate Growth and Division." Current Biology 14, no. 23 (December 2004): R1014—R1027. http://dx.doi.org/10.1016/j.cub.2004.11.027.

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42

Lipkin, M. "Growth and Development of Gastrointestinal Cells." Annual Review of Physiology 47, no. 1 (October 1985): 175–97. http://dx.doi.org/10.1146/annurev.ph.47.030185.001135.

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43

McCrum, Christopher L., and C. Thomas Vangsness. "Postmeniscectomy Meniscus Growth With Stem Cells." Sports Medicine and Arthroscopy Review 23, no. 3 (September 2015): 139–42. http://dx.doi.org/10.1097/jsa.0000000000000073.

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44

Gaudet, P., P. Fey, and R. Chisholm. "Growth and Maintenance of Dictyostelium Cells." Cold Spring Harbor Protocols 2008, no. 12 (December 1, 2008): pdb.prot5099. http://dx.doi.org/10.1101/pdb.prot5099.

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45

Martin, Bronwen, Randall Brenneman, Erin Golden, Tom Walent, Kevin G. Becker, Vinayakumar V. Prabhu, William Wood, Bruce Ladenheim, Jean-Lud Cadet, and Stuart Maudsley. "Growth Factor Signals in Neural Cells." Journal of Biological Chemistry 284, no. 4 (November 26, 2008): 2493–511. http://dx.doi.org/10.1074/jbc.m804545200.

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46

Ebendal, Ted, Peter L�nnerberg, Geng Pei, Annika Kylberg, Klas Kullander, H�kan Persson, and Lars Olson. "Engineering cells to secrete growth factors." Journal of Neurology 242, S1 (1994): S5—S7. http://dx.doi.org/10.1007/bf00939231.

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47

Ribatti, Domenico, and Enrico Crivellato. "Mast cells, angiogenesis, and tumour growth." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1822, no. 1 (January 2012): 2–8. http://dx.doi.org/10.1016/j.bbadis.2010.11.010.

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48

Pépin, Marie-France, Claude Chavarie, and Jean Archambault. "Growth and immobilization oftripterygium wilfordiicultured cells." Biotechnology and Bioengineering 38, no. 11 (December 20, 1991): 1285–91. http://dx.doi.org/10.1002/bit.260381105.

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49

Hu, Feihu, Xiu Wang, Gaofeng Liang, Lanxin Lv, Yanliang Zhu, Bo Sun, and Zhongdang Xiao. "Effects of Epidermal Growth Factor and Basic Fibroblast Growth Factor on the Proliferation and Osteogenic and Neural Differentiation of Adipose-Derived Stem Cells." Cellular Reprogramming 15, no. 3 (June 2013): 224–32. http://dx.doi.org/10.1089/cell.2012.0077.

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50

Hulley, Bonnie J., Marybeth Hummel, Linda L. Cook, Brita K. Boyd, and Sharon L. Wenger. "Trisomy 8 mosaicism: Selective growth advantage of normal cells vs. growth disadvantage of trisomy 8 cells." American Journal of Medical Genetics 116A, no. 2 (December 19, 2002): 144–46. http://dx.doi.org/10.1002/ajmg.a.10651.

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