Academic literature on the topic 'Transforming growth factors'

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Journal articles on the topic "Transforming growth factors"

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Hsuan, J. Justin. "Transforming growth factors β." British Medical Bulletin 45, no. 2 (1989): 425–37. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072332.

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Massagué, Joan. "The transforming growth factors." Trends in Biochemical Sciences 10, no. 6 (June 1985): 237–40. http://dx.doi.org/10.1016/0968-0004(85)90141-0.

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HELDIN, Carl-Henrik, and Bengt WESTERMARK. "Growth factors as transforming proteins." European Journal of Biochemistry 184, no. 3 (October 1989): 487–96. http://dx.doi.org/10.1111/j.1432-1033.1989.tb15041.x.

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Moses, Harold L., Jorma Keski-Oja, Robert J. Coffey, Russette M. Lyons, Nancy J. Sipes, and Charles C. Bascom. "Transforming growth factors and oncogenes." European Journal of Cancer and Clinical Oncology 23, no. 11 (November 1987): 1780. http://dx.doi.org/10.1016/0277-5379(87)90651-1.

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Lawrence, D. A. "Transforming growth factors-an overview." Biology of the Cell 53, no. 2 (1985): 93–98. http://dx.doi.org/10.1111/j.1768-322x.1985.tb00358.x.

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Stenn, Kurt S., Raymond L. Barnhill, and Yasmin Johnston. "Transforming growth factors and histopathologic interpretation." Journal of the American Academy of Dermatology 17, no. 1 (July 1987): 161–63. http://dx.doi.org/10.1016/s0190-9622(87)70185-6.

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Hammerman, M. R., S. A. Rogers, and G. Ryan. "Growth factors and metanephrogenesis." American Journal of Physiology-Renal Physiology 262, no. 4 (April 1, 1992): F523—F532. http://dx.doi.org/10.1152/ajprenal.1992.262.4.f523.

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The formation of all organs during embryogenesis, including kidney, is dependent on the timed and sequential expression of a number of polypeptide growth factors. Synthesis and actions of one or more members of the insulin-like growth factor, epidermal growth factor/transforming growth factor-alpha, transforming growth factor-beta, platelet-derived growth factor, fibroblast growth factor, and nerve growth factor families have been characterized in the developing metanephric kidney. Studies originating from a number of laboratories have defined the localization of growth factor mRNAs, receptors and peptides, have delineated patterns of growth factor synthesis, and have established the growth factor dependency of embryonic kidney development. The results of these investigations will be summarized in this editorial review and integrated within the broader context of growth factor cellular physiology and growth factor expression in nonrenal systems.
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Keski-Oja, Jorma, Edward B. Leof, Russette M. Lyons, Robert J. Coffey, and Harold L. Moses. "Transforming growth factors and control of neoplastic cell growth." Journal of Cellular Biochemistry 33, no. 2 (February 1987): 95–107. http://dx.doi.org/10.1002/jcb.240330204.

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Archer, J. R. "Ankylosing spondylitis, IgA, and transforming growth factors." Annals of the Rheumatic Diseases 54, no. 7 (July 1, 1995): 544–46. http://dx.doi.org/10.1136/ard.54.7.544.

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Gol-Winkler, R. "5 Paracrine action of transforming growth factors." Clinics in Endocrinology and Metabolism 15, no. 1 (February 1986): 99–115. http://dx.doi.org/10.1016/s0300-595x(86)80044-5.

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Dissertations / Theses on the topic "Transforming growth factors"

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Chung, Seung-Wook. "Modeling and analysis of the transforming growth factor beta signaling pathway." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 115 p, 2008. http://proquest.umi.com/pqdweb?did=1597632591&sid=15&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Porteous, C. "Epidermal growth factor, α-transforming growth factor and breast cancer." Thesis, University of Aberdeen, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383650.

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Evidence exists that epidermal growth factor (EGF) and alpha transforming growth factor (αTGF) are important in breast cancer. An inverse relationship between epidermal growth factor receptor (EGF-R) and oestrogen receptor (ER) has been reported by some, (1) but not all workers (2). The aim in this thesis was to develop assays to measure, levels of EGF, and determine EGF-R status in human breast tumours. These results were then correlated with each other, with ER and node status and histological grade (Bloom & Richardson). An additional aim in this thesis was to develop a source of αTGF in conditioned median (CM) from a transformed cell line. After extraction and purification, the αTGF was intended for use as an immunogen to produce a polyclonal antiserum which could be used in either an RIA or ELISA. EGF was measured by a radioimmunoassay (RIA) utilising a rabbit antimouse EGF antiserum. This assay (sensitivity 0.1ng/ml) was demonstrated to have no cross reactivity with αTGF. The EGF-R assay was similar to that described by Sainsbury. (1) In a series of 88 human breast tumours 47 (53.4%) were found to contain extractable EGF. Forty eight (54.5%) were EGF-R positive and 39 (44.3%) were ER positive. A direct relationship between EGF and ER+ ve status was found (p < 0.01). Significantly higher levels of EGF were extracted from ER+ ve tumours (p = 0.049) compared with that from ER-ve tumours. However no relationship between EGF-R and EGF or ER status was found, or between EGF levels and histological grade or node status. A suitable cell line which produced αTGF, was obtained and culture conditions optimised. Alpha-TGF was assayed by a radioreceptor assay which utilised a cell line rich in EGF-R (A431). Extraction of αTGF was based on the principles of molecular grading by gel filtration (Sephadex G50), and ion exchange (Sephadex CM C25). By this process the αTGF was purified and separated it from any EGF present. By this method 20μg of αTGF was produced from 61t of CM. 1) Sainsbury JRC, Farndon JR, Serbet GV, Harris AL. Epidermal-growth-factor-receptors and oestrogen receptors in human breast cancer. Lancet 1985; 1: 364-368. 2) Fitzpatrick SL, Brightwell J, Wattliff JL, Barrows GH, Schultz GS. Epidermal growth factor binding by breast tumour biopsies and relationship to oestrogen receptor and progestin receptor levels. Cancer Res 1984; 44: 3448-3453.
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Smith, Cheryl A. "Skeletal muscle injury, fibrosis and transforming growth factor-[beta]." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1744.

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Thesis (Ph. D.)--West Virginia University, 2000.
Title from document title page. Document formatted into pages; contains xii, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Gu, Ye. "Homo & heterodimeric TGF-[beta] family growth factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610106.

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Lanxon-Cookson, Erinn Claire. "Lovastatin decreases TGF-ß1 concentration of glomerular endothelial cells cultured in high glucose." Online access for everyone, 2008. http://www.dissertations.wsu.edu/Thesis/Spring2008/e_lanxon_cookson_040308.pdf.

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Zhang, Min Fen. "The role of milk transforming growth factor-[beta](TGF-[beta]) in the development of the infant gut and gut mucosal immune system." Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phz51.pdf.

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In title, [beta] is represented by the Greek letter. Copies of author's previously published articles inserted. Errata pages pasted onto back end-paper. Bibliography: leaves 104-137. Studies milk TGF-[beta] and its receptors in the post-natal gut using a rat model to investigate a link between milk TGF-[beta] and the development of the infant gut and gut mucosal immune system. Finds maternal milk may be a major source of TGF-[beta] to the immature gut and may react with receptors on the cells of the mucosal immune system along the gastro-intestinal tract, modulating infant mucosal immune responses in the transition to the post-natal enteral feeding.
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Pascal, M. M. "The role of transforming growth factor beta and other growth factors in the development of diabetic retinopathy." Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593270.

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The present study showed that TFG-β mRNA and protein expression is regulated by glucose concentration in HREC. Maximal secreted protein levels and mRNA were produced at a concentration of 15 mM and the majority of the TGF-β is found in an active form in these cells. These results were novel and specific as HREC have not been shown before to express TFG-β in response to glucose. TGF-β appears to be central to a wide range of pathological features involved in the disease and this first study highlights a possible important role for TGF-β in the mechanism of induction of microvascular abnormalities in the retina. It could also play a role as a key mediator of the high glucose induced effects in DR, as is the case in the kidney. Glucose dependent changes in TGF-β receptors expression and signalling intermediates were also examined in HREC. These studies indicate that glucose is able to regulate both TGF-β expression and the receptor numbers of affinity but it is apparent that there is no simple correlation between secreted TGF-β and receptor number or affinity or expression. Protein kinase C isoforms protein expression did not change relatively to glucose but various isoforms were expressed at different intensities in endothelial cells and TGF-β signalling cascade involves a MAPK independent pathway. TGF-β expression in the ganglion cell layer demonstrated a neurotrophic role for TGF-β, whereas VEGF expression did not seem to correlate spatially or temporally with angiogenesis. We suggest that both systemic cells (PBLs) and endothelial cells are able to secrete a wide range of growth factors when activated by glucose. These factors, along with other ones (platelet derived growth factor or insulin like growth factor type 1), may act in synergy to produce an imbalance in growth factor levels which could lead to angiogenesis and therefore contribute to the pathogenesis of PDR.
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Kam, Siu-kei Christy. "The role of TGF-[beta] signaling in the initiation of TNF-[beta] expression in human PBMC derived macrophages." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38746049.

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Kam, Siu-kei Christy, and 甘笑琪. "The role of TGF-{221} signaling in the initiation of TNF-α expression in human PBMC derived macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38746049.

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Ni, Xueying. "Activin and a putative novel activin receptor-like kinase in the human placenta." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ39215.pdf.

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Books on the topic "Transforming growth factors"

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Rik, Derynck, and Miyazono Kōhei 1956-, eds. The TGF-[beta] family. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2008.

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A, Piez Karl, and Sporn Michael B, eds. Transforming growth factor-[beta]s: Chemistry, biology, and therapeutics. New York, N.Y: New York Academy of Sciences, 1990.

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Phillips, John L. Regulation of cytokine production in the rat osteoblast by tansforming growth factor-BETA. [s.l: s.l.], 1992.

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1949-, Breit Samuel N., and Wahl Sharon M, eds. TGF-Ý and related cytokines in inflammation. Basel: Birkhäuser, 2001.

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Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?]: U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.

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Ivashchenko, I͡U. D.(I͡Uriĭ Dmitrievich). Polipeptidnye faktory rosta i kant͡serogenez. Kiev: Nauk. dumka, 1990.

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Wager, Ruth Ellen. A phorbol ester-regulated ribonuclease system controlling transforming growth factor-B1 gene expression in hematopoietic cells. [New York]: [Columbia University], 1992.

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Benson, John R. TGF [beta] and cancer. Austin: R.G. Landes, 1998.

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L, Moses Harold, Lengyel Peter 1929-, Stiles Charles D, and Genentech Inc, eds. Growth inhibitory and cytotoxic polypeptides ; proceedings of a Genentech-Smith, Kline & French-Triton Biosciences-UCLA Symposium held in Keystone, Colorado, January 24-30, 1988. New York: A.R. Liss, 1989.

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M, Glover David, Hall A, and Hastie Nicholas, eds. Cell biology of cancer. Cambridge, Eng: Company of Biologists Ltd., 1994.

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Book chapters on the topic "Transforming growth factors"

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Pfeilschifter, J. "Transforming Growth Factor-β." In Growth Factors, Differentiation Factors, and Cytokines, 56–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_5.

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Schomberg, David W., and George W. Mulheron. "Transforming Growth Factors and Ovarian Function." In Growth Factors in Reproduction, 79–90. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3162-2_6.

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Daniel, Charles W., and Gary B. Silberstein. "Mammary Growth Regulation by Transforming Growth Factor β." In Growth Factors in Reproduction, 115–28. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3162-2_9.

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Heldin, Carl-Henrik, and Bengt Westermark. "Growth factors as transforming proteins." In EJB Reviews 1989, 119–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-75189-9_8.

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Moses, H. L., J. Keski-Oja, R. M. Lyons, N. J. Sipes, C. C. Bascom, and R. J. Coffey. "Biological effects of transforming growth factors." In Advances in Growth Hormone and Growth Factor Research, 191–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-11054-6_13.

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Roberts, A. B., and M. B. Sporn. "The Transforming Growth Factor-βs." In Peptide Growth Factors and Their Receptors I, 419–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_8.

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Roberts, A. B., and M. B. Sporn. "The Transforming Growth Factor-βs." In Peptide Growth Factors and Their Receptors I, 419–72. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_8.

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Akhurst, Rosemary J., Marion Dickson, and Fergus A. Millan. "Transforming growth factor ßs and cardiac development." In Growth Factors and the Cardiovascular System, 347–66. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3098-5_21.

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Flanders, Kathleen C., Belinda A. Marascalco, Anita B. Roberts, and Michael B. Sporn. "Transforming Growth Factor β: A Multifunctional Regulatory Peptide with Actions in the Reproductive System." In Growth Factors in Reproduction, 23–37. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3162-2_2.

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Lobb, Derek K., and Jennifer H. Dorrington. "Bovine Thecal Cells Secrete Transforming Growth Factor α and β." In Growth Factors and the Ovary, 199–203. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5688-2_19.

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Conference papers on the topic "Transforming growth factors"

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Kmyta, Vladyslava, and Liudmyla Prystupa. "Transforming growth factor-ß1 and Matrix Metalloproteinase-9 as factors of airway remodeling among asthmatic patients." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5053.

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O’Conor, Christopher J., Kenneth W. Ng, Lindsay E. Kugler, Gerard A. Ateshian, and Clark T. Hung. "The Response of Tissue Engineered Cartilage to the Temporal Application of Transforming and Insulin-Like Growth Factors." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176523.

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Agarose has been used as an experimental scaffold for cartilage tissue engineering research due to its biocompatibility with chondrocytes, support of cartilage tissue development, and ability to transmit mechanical stimuli [1–3]. Tissue engineering studies have demonstrated that the temporal application of transforming growth factor (TGF) β3 for only 2 weeks elicits rapid tissue development that results in mechanical properties approaching native values [4]. However, it is not known whether this response to a 2-week exposure to growth factors is unique to TGF-β3. Therefore, the present study characterizes the response of tissue engineered cartilage to the temporal application of the anabolic growth factors TGF-β1, TGF-β3, and insulin-like growth factor I (IGF-I).
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Epstein Shochet, Gali, Becky Bardenstein-Wald, Elizabetha Brook, and David Shitrit. "Transforming growth factor beta (TGF-ß) pathway activation by IPF fibroblast-derived soluble factors is mediated by IL-6 trans-signaling." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3352.

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Hu, C. J., A. Laux, L. Wang, H. Zhang, M. G. Frid, S. Kumar, S. Riddle, M. Li, and K. R. Stenmark. "Hypoxia, Cytokines, and Growth Factors Exhibit Distinct and Synergistic Roles in Transforming Normal Pulmonary Fibroblasts into Persistently Activated Fibroblasts." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1923.

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Yang, Yueh-Hsun, and Gilda A. Barabino. "Interrupted Treatment With Growth Factors in Combination With Hydrodynamic Forces Enhances ECM Deposition in Tissue-Engineered Cartilage." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53282.

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Achievement of viable engineered tissues through in-vitro cultivation in bioreactor systems requires a thorough understanding of the complex interplay between mechanical forces and biochemical cues. Briefly, bioreactors have been employed to impart mechanical stimuli to support tissue growth and development. Continuous fluid-induced shear stress, for example, has been shown to influence morphology and properties of engineered cartilage.1 Fluid flow enhances mass transfer mechanisms and simultaneously provides mechanical stimuli across or through the construct to emulate shear forces that occur in the knee or other joints. Critical biochemical factors, such as growth factors, are secreted by cells2,3 and involved in cell-to-cell signaling. Guided by these molecules, cells can communicate with each other and work synergistically to accomplish a specific task. It has also been demonstrated that the pathways of certain growth factors, such as transforming growth factor-β (TGF-β) family and insulin-like growth factor-1 (IGF-1), are responsive to shear stress, resulting in enhanced cell and tissue activities, and their expression is also up-regulated by fluid-induced shear stress.4,5 This evidence suggests their involvement in mechanotransduction mechanisms. However, a combination of mechanical and biochemical stimuli results in a complex culture environment which is not yet fully characterized. The present study was designed to obtain an understanding of the combined effects of hydrodynamic forces and growth factors on cartilage regeneration by employing a custom-designed wavy-walled bioreactor1 (WWB) and by selecting IGF-1 and TGF-β1 as two model molecules. We hypothesized that bioprocessing conditions which optimize mechanical, biochemical and compositional properties of tissue-engineered cartilage can be achieved under hydrodynamic stimuli in combination with an appropriate use of IGF-1 or TGF-β.
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Chung, Eunna, and Marissa Nichole Rylander. "Effects of Growth Factors and Stress Conditioning on the Induction of Heat Shock Proteins and Osteogenesis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206662.

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Tissue engineering is an emerging field that focuses on development of methods for repairing and regenerating damaged or diseased tissue. Successful development of engineered tissues is often limited by insufficient cellular proliferation and insufficient formation of extracellular matrix. To induce effective bone regeneration, many research groups have investigated the cellular response and capability for tissue regeneration associated with bioreactor conditions and addition of growth factors [1]. Bioreactors in tissue engineering have been developed to expose cells to a similar stress environment as found within the body or induce elevated stress levels for potential induction of specific cellular responses associated with tissue regeneration. Native bone encounters a diverse array of dynamic stresses such as shear, tensile, and compression daily. Stress conditioning protocols in the form of thermal or tensile stress have been shown to induce up-regulation of molecular chaperones called heat shock proteins (HSPs) and bone-related proteins like MMP13 (matrix metallopeptidase 13) [2] and OPG (osteoprotegerin) [3, 4]. HSPs have important roles in enhancing cell proliferation and collagen synthesis. Osteogenic growth factors such as TGF-β1 (transforming growth factor beta 1) and BMP-2 (bone morphogenetic protein 2) are related to bone remodeling and osteogenesis as well as HSP induction [5]. Therefore, identification of effective preconditioning using growth factors and stress protocols that enhance HSP expression could substantially advance development of bone regeneration. The purpose of this research was to identify preconditioning protocols using osteogenic growth factors and tensile stress applied through a bioreactor system to enhance expression of HSPs and bone-related proteins while minimizing cellular injury for ultimate use for bone regeneration.
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Caggia, Silvia, Saverio Candido, Massimo Libra, and Venera Cardile. "Abstract 4074: Transcription factors involved in the genesis and progression of cancer differently modulated by transforming growth factor-beta3 (TGF-Beta3) in prostate cell lines." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4074.

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Lacroix, Valéry, Afaf Bouydo, Genshichiro Katsumata, Yinsheng Li, and Kunio Hasegawa. "Proposal of a New Subsurface-to-Surface Flaw Transformation Rule for Fatigue Crack Growth Analyses." In ASME 2017 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/pvp2017-66049.

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When a subsurface flaw is located near the component free surface, the first step consists of characterizing the flaw as surface or subsurface in compliance with subsurface-to-surface flaw proximity rules. The re-characterization process from subsurface to surface flaw is addressed in all Fitness-for-Service (FFS) Codes. However, the specific criteria for the rules on transforming subsurface flaws to surface flaws are different among the FFS Codes. This re-characterization concept is essential and important for subsurface flaws in the flaw assessment procedures. It is applied for three stages of the flaw assessment: at service inspection for flaw characterization, at subcritical crack growth calculation, such as fatigue crack growth, and at ductile/brittle fracture assessment. In this frame, fatigue crack growth experiments were recently conducted by the authors and it was highlighted that the subsurface-to-surface transformation is highly sensitive to the aspect ratio a/l of the flaw whereas the proximity factors in the rules are defined by constant values i.e., regardless of the flaw aspect ratios a/l. The authors have therefore proposed a new subsurface-to-surface flaw proximity rule based on experimental data and equivalent fatigue crack growth rates. Then, the authors demonstrated through numerous Fatigue Crack Growth (FCG) calculations that the current ASME B&PV Code Section XI surface proximity factor should be updated according to the type of component i.e., piping or vessel. The paper summarizes all the steps leading to the improvement of the ASME Code Section XI subsurface-to-surface proximity rule, from the fatigue crack growth experiments to the studies of the suitability of the current flaw-to-surface proximity factor. Furthermore, based on additional fatigue crack growth calculations and more refined investigations, the paper proposes finally a new limit value for the surface proximity factor. As a result, a proposal for modification of the ASME Code Section XI, Appendix C is provided. The paper is used for the technical basis of this proposal.
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Heo, Su-Jin, Tristan P. Driscoll, and Robert L. Mauck. "Dynamic Tensile Loading Activates TGF and BMP Signaling in Mesenchymal Stem Cells on Aligned Nanofibrous Scaffolds." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80706.

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Mesenchymal stem cells (MSCs) are a promising cell source for tissue engineering applications, given their ease of isolation and multi-potential differentiation capacity [1]. External mechanical cues directly influence MSC lineage commitment [2]. However, it is not yet clear how these physical cues are transduced to the cell nucleus, an understanding of which may prove essential for orthopaedic tissue engineering. Transforming growth factor beta (TGFβ) and bone morphogenetic protein (BMP), members of the TGF beta superfamily, regulate cellular processes including growth and differentiation [3, 4]. TGF and/or BMP ligand binding initiate SMAD phosphorylation, translocation to the nucleus, and transcriptional activation of target genes [4]. Additionally, both ligands can influence the organization of chromatin and the Lamin A/C (LMAC) nucleoskeletal network [5]. For example, we have recently shown that TGF-β3 leads to corticalized LMAC, marked increases in heterochromatin (HTC), and increased nuclear stiffness [6]. Interestingly, dynamic tensile stretch of MSCs on aligned nanofibrous scaffolds, in the absence of these differentiation factors, resulted in many of these same nuclear transformations [6, 7]. The objective of this study was to identify how dynamic tensile stress is transduced in MSCs on aligned nanofibrous scaffolds, and further, to ascertain whether these mechanoregulatory changes are coordinated through TGFβ/BMP signaling pathways.
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Reza, Anna T., and Steven B. Nicoll. "Chemically Defined Medium With TGF-β3 Enhances Matrix Elaboration by Nucleus Pulposus Cells Encapsulated in Novel Photocrosslinked Carboxymethylcellulose Hydrogels." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206199.

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Back pain is a significant clinical concern often attributed to degeneration of the intervertebral disc (IVD) and the associated dehydration of the nucleus pulposus (NP) [1]. The NP is a gel-like tissue at the center of the disc, rich in proteoglycans and type II collagen that functions to resist compressive forces through the generation of a hydrostatic swelling pressure [2]. Tissue engineering strategies may provide a viable NP replacement therapy as an alternative to current surgical procedures. However, several factors including medium formulation and scaffold selection can affect construct maturation [3]. For example, transforming growth factor-beta 3 (TGF-β3) has been shown to enhance the functional properties of tissue engineered cartilage constructs, with more pronounced results observed in serum-free conditions [3]. NP cells are commonly cultured in ionically crosslinked alginate hydrogels to maintain their phenotypic properties; however, these scaffolds have been shown to lose structural integrity over time, creating a need for an alternative biomaterial [4]. Therefore, the objective of this study was to examine the effects of medium formulation on NP cells encapsulated in novel photocrosslinked carboxymethylcellulose (CMC) hydrogels.
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Reports on the topic "Transforming growth factors"

1

Reiss, Michael. Transforming Growth Factor-B Receptors in Humans. Fort Belvoir, VA: Defense Technical Information Center, January 2001. http://dx.doi.org/10.21236/ada393526.

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2

Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.

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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.
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3

Boye, Greta, and Winston Ramautarsing. Revitalizing Agriculture in Suriname. Inter-American Development Bank, May 1997. http://dx.doi.org/10.18235/0008717.

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Suriname faces unprecedented challenges in transforming its agricultural sector to a market based system, and it will need to offset the deterioration of the sector resulting from the probable loss of its preferential markets in the next decade. This study seeks to contribute to the understanding of the measures that are necessary to address the constraints on agricultural growth and development. The analysis builds on discussions that took place in May 1996 with government officials, representatives of private sector organizations and international agencies. Based on field work and subsequent analyses, this report offers recommendations on actions needed to sustain and enhance the growth of Surinam¿s existing export products, promote the emergence of promising new products, and strengthen institutions that support both of those activities. The study includes a general introduction and background information on the contribution of agriculture to the economy and the performance of agriculture, the main constraints on the growth and development of the sector, key factors affecting competitiveness, Government¿s plans for development in the area and, finally a strategy for revitalizing the agricultural sector in Suriname. The rationale for revitalizing the agricultural sector is to increase national income ad to foster the economic and social development of Suriname. Since agriculture is a sector of vital importance to the Surinamese economy, it provides a good vehicle for achieving this aim.
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4

Nickerson, Nicole. Transforming Growth Factor Beta Signaling in Growth of Estrogen-Insensitive Metastatic Bone Lesions. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada558405.

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5

Oursler, Merry J. Transforming Growth Factor B Regulation of Tumor Progression in Metastatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395849.

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6

Oursler, Merry Jo. Transforming Growth Factor Beta Regulation of Tumor Progression in Metastatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427069.

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7

Chung, Lee. Expression of Transforming Growth Factor-Beta (TGF-B) in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada405312.

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8

Bhowmick, Neil A., and Harold Moses. Regulated Transformation of Mammary Epithelial Cells by Transforming Growth Factor-Beta 1. Fort Belvoir, VA: Defense Technical Information Center, March 2002. http://dx.doi.org/10.21236/ada405576.

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9

Bhowmick, Neil A., and Harold Moses. Regulated Transformation of Mammary Epithelial Cells by Transforming Growth Factor Beta 1. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada415783.

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10

Nyman, Jeffry S. Targeting Transforming Growth Factor Beta to Enhance the Fracture Resistance of Bone. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada571744.

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