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Littérature scientifique sur le sujet « Bone cells Metabolism »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 28 janvier 2023

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Articles de revues sur le sujet "Bone cells Metabolism"

1

INOUE, HIROMASA. "Cells phagocytizing bone. Bone metabolism and osteoclast." Kagaku To Seibutsu 23, no. 2 (1985): 99–102. http://dx.doi.org/10.1271/kagakutoseibutsu1962.23.99.

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Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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Locci, P., E. Becchetti, G. Venti, C. Lilli, L. Marinucci, E. Donti, G. Paludetti, and M. Maurizi. "Glycosaminoglycan metabolism in otosclerotic bone cells." Biology of the Cell 86, no. 1 (1996): 73–78. http://dx.doi.org/10.1111/j.1768-322x.1996.tb00958.x.

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Barry, Patrick. "Skeletal discovery: Bone cells affect metabolism." Science News 172, no. 6 (September 30, 2009): 83. http://dx.doi.org/10.1002/scin.2007.5591720602.

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Motyl, Katherine J., Anyonya R. Guntur, Adriana Lelis Carvalho, and Clifford J. Rosen. "Energy Metabolism of Bone." Toxicologic Pathology 45, no. 7 (October 2017): 887–93. http://dx.doi.org/10.1177/0192623317737065.

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Biological processes utilize energy and therefore must be prioritized based on fuel availability. Bone is no exception to this, and the benefit of remodeling when necessary outweighs the energy costs. Bone remodeling is important for maintaining blood calcium homeostasis, repairing micro cracks and fractures, and modifying bone structure so that it is better suited to withstand loading demands. Osteoclasts, osteoblasts, and osteocytes are the primary cells responsible for bone remodeling, although bone marrow adipocytes and other cells may also play an indirect role. There is a renewed interes

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Kumegawa, Masayoshi. "Role of Bone Cells in Bone Metabolism : Osteoclasts and Osteocytes." Journal of the Kyushu Dental Society 48, no. 5 (1994): 640–43. http://dx.doi.org/10.2504/kds.48.640.

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Ruzicska, Éva, and Gyula Poór. "Diabetes and bone metabolism." Orvosi Hetilap 152, no. 29 (July 2011): 1156–60. http://dx.doi.org/10.1556/oh.2011.29147.

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In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through co

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Anderson, Paul H., Gerald J. Atkins, Andrew G. Turner, Masakazu Kogawa, David M. Findlay, and Howard A. Morris. "Vitamin D metabolism within bone cells: Effects on bone structure and strength." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 42–47. http://dx.doi.org/10.1016/j.mce.2011.05.024.

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Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increase

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Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increase

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Thèses sur le sujet "Bone cells Metabolism"

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Mason, Rachel Ann. "Effects of estrogens and androgens on bone cell metabolism /." Title page, table of contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phm411.pdf.

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Secreto, Frank. "The regulation of arachidonic acid metabolism in human osteoblast-like cells." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2970.

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Thesis (Ph. D.)--West Virginia University, 2003.<br>Title from document title page. Document formatted into pages; contains vi, 123 p. : ill. Includes abstract. Includes bibliographical references (p. 110-123).

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Macoritto, Michael. "Mechanisms of vitamin D receptor and retinoid X receptor mediated hormone resistance and cell differentiation in normal and cancer cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111887.

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Vitamin D is a precursor to a steroid hormone, 1,25 dihydroxyvitamin D (1,25(OH)2D). After its discovery and the characterization of its receptor, the vitamin D receptor (VDR), it was initially thought only to be involved in calcium homeostasis, but further research revealed an important role for vitamin D in the regulation of cell growth and differentiation of such cells as osteoblasts and bone marrow adipocytes. 1,25(OH)2D has also been shown to be a strong inhibitor and pro-differentiator of keratinocytes. The anti-proliferative and pro-differentiative properties of this hormone have led to

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Star, Gregory. "The effects of bone morphogenic proteins and transforming growth factor [beta] on in-vitro endothelin-1 production by human pulmonary microvascular endothelial cells /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111942.

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Introduction: Idiopathic Pulmonary arteriole hypertension (IPAH) is a rare but severely debilitating disease that strikes women to men at a ratio of 3:1. Endothelial cell (EC) dysfunction is a hallmark of the disease. This includes rapid growth of the ECs until the occlusion of the vasculature as well as decreased blood levels of vasodilators. Markedly increased levels of endothelin-1, a potent vasoconstrictor and smooth muscle mitogen, have been noted in IPAH patients.<br>Recently mutations in the bone morphogenic protein receptor type II (BMPRII) have been linked to the disease. Interestingl

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Ren, Song. "Metabolism of cyclophosphamide : implications for hematopoietic stem cell transplantation /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/7968.

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Pan, Beiqing. "Mechanisms of skeletal disease mediated by haematological malignancies /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09php1871.pdf.

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Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine and The Hanson Centre, Institute of Medical and Veterinary Science, 2004.<br>"August 2004" Errata inside front cover. Bibliography: leaves 126-159.

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Zarrinkalam, Krystyna. "Characterisation of osteoblast function in a feline model of mucopolysaccharidosis type VI." Title page, contents and introduction only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phz38.pdf.

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Addenda slip inserted in back. Includes bibliographical references (leaves 178-231). To further the understanding of the molecular mechanisms that contribute to the skeletal pathology of mucopolysaccharidosis type VI and to investigate the production of organic matrix by mucopolysaccharidosis VI osteoblasts

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Pan, Beiqing. "Molecular and cellular studies of zoledronic acid : a potent inhibitor of multiple myeloma-induced osteolysis." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09MSM/09msmp187.pdf.

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Bibliography: leaves 86-103. Investigates the effect of zoledronic acid on myeloma cells and osteoblast-like cells to establish the molecular and cellular mechanisms responsible for the clinical effectiveness of bisphosphonates in the treatment of patients with myelomatosis. Concludes that zoledronic acid inhibits myelomatosis-induced osteolysis thorugh the mechanisms of myeloma cell death and proliferation and maturation of osteoblasts.

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Freitas, Claudia Mercedes. "Regulation of Immune Cell Activation and Functionby the nBMPp2 Protein andthe CD5 Co-Receptor." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8257.

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According to the centers for disease control and prevention (CDC) and the world healthorganization (WHO), heart disease and immune related diseases such as diabetes and cancer areamong the leading causes of death around the world. Thus, the regulation of the function ofimmune cell plays a key role in health and disease. Calcium (Ca2+) ions play a critical role inimmune cell activation, function and in a robust immune response. Defects in Ca2+ signalinginfluences the development of cardiac disease, Alzheimer disease, immune cell metabolism,muscle dysfunction, and cancer. Each immune cell is uni

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Laketic-Ljubojevic, Ira. "Glutamate signalling in bone cells." Thesis, University of York, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311080.

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Livres sur le sujet "Bone cells Metabolism"

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Dean, Buckner C., and Clift R. A, eds. Technical and biological components of marrow transplantation. Boston: Kluwer Academic Publishers, 1995.

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European Symposium on Calcified Tissues (20th 1987 Sirmione, Italy). XX European Symposium on Calcified Tissues, Sirmione, Italy, October 4-8, 1987: Abstracts, including Satellite Workshop on Molecular and Cell Biology and Satellite Workshop on Biology and Regulation of Bone Metabolism : Clinical Significance. New York: Springer International, 1987.

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McCann, Shaun R. Red blood cells. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0004.

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Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the

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Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)

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Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.

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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the

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Skiba, Grzegorz. Fizjologiczne, żywieniowe i genetyczne uwarunkowania właściwości kości rosnących świń. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_gs_2020.

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Bones are multifunctional passive organs of movement that supports soft tissue and directly attached muscles. They also protect internal organs and are a reserve of calcium, phosphorus and magnesium. Each bone is covered with periosteum, and the adjacent bone surfaces are covered by articular cartilage. Histologically, the bone is an organ composed of many different tissues. The main component is bone tissue (cortical and spongy) composed of a set of bone cells and intercellular substance (mineral and organic), it also contains fat, hematopoietic (bone marrow) and cartilaginous tissue. Bones a

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Bower, Mark, Louise Robinson, and Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.

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Cancer produces endocrine and metabolic complications in two ways. Firstly, the primary tumour or its metastases may interfere with the function of endocrine glands, kidneys, or liver by invasion or obstruction. Secondly, tumours may give rise to remote effects without local spread and these actions are termed paraneoplastic manifestations of malignancy. Generally, these paraneoplastic syndromes arise from secretion by tumours of hormones, cytokines, and growth factors, but also occur when normal cells secrete products in response to the presence of tumour. This chapter reviews the pathogenesi

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Studies of intercellular communication and intracellular metabolic responses by bone cells to simulated weightlessness: Final NASA report. [Washington, DC: National Aeronautics and Space Administration, 1997.

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United States. National Aeronautics and Space Administration., ed. Studies of intercellular communication and intracellular metabolic responses by bone cells to simulated weightlessness: Final NASA report. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Clift, Reginald, and C. Dean Buckner. Technical and Biological Components of Marrow Transplantation. Springer, 2012.

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Chapitres de livres sur le sujet "Bone cells Metabolism"

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Pignolo, Robert J., and Moustapha Kassem. "Circulating Osteogenic Cells." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 111–18. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch14.

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Gruber, Harry E., Kim D. Finley, Lori A. Luchtman, Robert M. Hershberg, Scott S. Katzman, Paul K. Laikind, Erik N. Meyers, et al. "Insertion of Hypoxanthine Phosphoribosyltransferase cDNA into Human Bone Marrow Cells by a Retrovirus." In Purine and Pyrimidine Metabolism in Man V, 171–75. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5104-7_27.

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Sraer, Josée, Marcelle Bens, Jean-Paul Oudinet, and Larent Baud. "Arachidonic Acid Metabolism During Interactions Between Glomerular and Bone Marrow-Derived Cells." In Advances in Experimental Medicine and Biology, 23–47. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5700-1_2.

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Bourgeais, Jérôme, and Olivier Hérault. "In Vitro Analysis of Energy Metabolism in Bone-Marrow Mesenchymal Stromal Cells." In Methods in Molecular Biology, 59–70. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1425-9_5.

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Braess, J., D. Berkovic, M. Feuring-Buske, E. Fleer, J. Pförtner, C. Wegendt, S. Keye, et al. "AraC Metabolism in Fresh Leukemic Blasts/ Normal Bone Marrow/ Hematopoetic Stem Cells and its Impact on the Lipid Composition of Leukemic Cells (HL60)." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 596–602. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71960-8_80.

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Boyce, Brendan F. "Bone and Immune Cell Interactions." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 1036–42. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch124.

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Reuter, Christoph, Claus Rolf, Eberhard Schleyer, Michael Unterhalt, Bernhard Woermann, Thomas Buechner, and Wolfgang Hiddemann. "Differential Effect of GM-CSF on the Intracellular Ara-C Metabolism in Normal Bone Marrow Mononuclear Cells and Acute Myeloid Leukemia (AML) Blasts." In Acute Leukemias V, 41–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-78907-6_6.

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Dziak, Rosemary. "Prostaglandins as Mediators of Bone Cell Metabolism." In Calcium in Biological Systems, 533–39. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2377-8_57.

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Ikeogu, Nnamdi M., Chidalu A. Edechi, Gloria N. Akaluka, Aida Feiz-Barazandeh, and Jude E. Uzonna. "Isolation and Preparation of Bone Marrow-Derived Immune Cells for Metabolic Analysis." In Methods in Molecular Biology, 273–80. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0802-9_19.

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Stone, Michael, and Connie Weaver. "Improving Human Nutrition: A Critical Objective for Potassium Recommendations for Agricultural Crops." In Improving Potassium Recommendations for Agricultural Crops, 417–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-59197-7_15.

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AbstractPotassium (K) is the most abundant cation in intracellular fluid where it plays a key role in maintaining cell function. The majority of K consumed (60–100 mmol day−1) is lost in the urine, with the remaining excreted in the stool, and a very small amount lost in sweat. Little is known about the bioavailability of K, especially from dietary sources. Less is understood on how bioavailability may affect health outcomes. Potassium is an essential nutrient that has been labeled a shortfall nutrient by recent Dietary Guidelines for Americans Advisory Committees. Increases in K intake have been linked to improvements in cardiovascular and other metabolic health outcomes. There is growing evidence for the association between K intake and blood pressure (BP) reduction in adults; hypertension (HTN) is the leading cause of the cardiovascular disease (CVD) and a major financial burden (US$53.2 billion) to the US public health system and has a significant impact on all-cause morbidity and mortality worldwide. Evidence is also accumulating for the protective effect of adequate dietary K on age-related bone loss and glucose control. Understanding the benefit of K intake from various sources may help to reveal how specific compounds and tissues influence K movement within the body, and further the understanding of its role in health.

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Actes de conférences sur le sujet "Bone cells Metabolism"

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Zhou, Xiaozhou, John E. Novotny, and Liyun Wang. "Modeling Fluorescence Recovery After Photobleaching in Cyclically Loaded Bone: Potential Application in Quantitatively Measuring Load-Induced Solute Flows." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193018.

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Recent experiments strongly suggest that osteocytes, the most numerous bone cells, play much more active roles in bone adaptation and metabolism [1]. These multifunctioning cells are found to detect external mechanical stimuli, and to release soluable agents that modulate the functioning of other cell types [1, 2]. Solute transport around osteocytes through the bone lacunar-canalicular system (LCS), especially via load-induced convection, is critical for osteocyte viability and proper functioning. However, despite of significant advance in elucidating the LCS microstructure, permeability, and

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Li, Xiang-Qin, Ke-Dong Song, and Tian-Qing Liu. "Growth and Metabolism of Bone Marrow Mesenchymal Stem Cells within Collagen Scaffolds in a Novel Bioreactor." In 2015 International Conference on Medicine and Biopharmaceutical. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789814719810_0037.

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Tate, Melissa L. Knothe, and Peter Niederer. "A Theoretical FE-Based Model Developed to Predict the Relative Contribution of Convective and Diffusive Transport Mechanisms for the Maintenance of Local Equilibria Within Cortical Bone." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0808.

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Abstract Whereas diffusion has been shown to be the major contributing mechanism for mass transfer in the extravascular spaces of organs and soft tissues, it is unlikely that diffusion alone can account for sufficient molecular transport in the porous yet relatively impermeable tissue of cortical bone. An alternate mechanism for such mass transfer is intrinsic to the functional role of cortical bone in transferring loads within the musculoskeletal system. Namely, it has been proposed that mechanical loading causes minute deformations within the poroelastic tissue of cortical bone, resulting in

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Trucco, Matteo, Nino Rainsusso, Piti Techavichit, Ronald Bernardi, Ryan Shuck, Laura Satterfield, Wendy Allen-Rhoades, Larry Donehower, David Loeb, and Jason Yustein. "Abstract A70: Targeting pediatric bone sarcoma stem cell with metabolic inhibitors." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a70.

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Takai, Erica, Clark T. Hung, Aurea Tucay, Djordje Djukic, Mary L. Linde, Kevin D. Costa, James T. Yardley, and X. Edward Guo. "Design of a Microfluidic System for 3D Culture of Osteocytes In Vitro." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33229.

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Bone adapts to its mechanical environment so that its form follows function, a mechanism known as Wolff’s law, or bone adaptation. Although the basic concepts of Wolff’s law have been generally accepted, the regulatory signals and the underlying cellular and molecular pathways, which mediate this adaptive process, are unknown. Failure of normal bone adaptation plays a significant role in the etiology of metabolic bone diseases such as osteoporosis and osteopetrosis, bone loss in space flight and failure of total joint replacements. During the past three decades, there have been extensive in vi

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Penninger, Charles L., Neal M. Patel, and Andrés Tovar. "A Novel HCA Framework for Simulating the Cellular Mechanisms of Bone Remodeling." In ASME 2012 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/detc2012-70613.

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Each year, bone metabolic diseases affect millions of people of all ages, genders, and races. Common diseases such as osteopenia and osteoporosis result from the disruption of the bone remodeling process and can place an individual at a serious fracture risk. Bone remodeling is the complex process by which old bone is replaced with new tissue. This process occurs continuously in the body and is carried out by bone cells that are regulated by numerous metabolic and mechanical factors. The remodeling process provides for various functions such as adaptation to mechanical loading, damage repair,

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Horiguchi, Atsushi, and Toshihiko Shiraishi. "Study on a Cell Mechanosensing System by Measuring Structural Deformation and Biochemical Response." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-51456.

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Mechanical stimulation induces new bone formation in vivo and promotes the metabolic activity and the gene expression of osteoblasts in vitro. It was reported that biochemical signals of osteoblasts to sense mechanical stimulation are activated according to their actin cytoskeletal deformation. However, there have been not so many researches on the relationship between cytoskeletal deformation and biochemical response. Here we show an original method to investigate a cell mechanosensing system and the quantitative relationship between the deformation of cytoskeletal structure and the change of

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Zhu, Shiya, Akanksha Mahajan, Sung-Hyeok Hong, Susana Galli, Congyi Lu, You-Shin Chen, Sara Misiukiewicz, Stacey Chung, Jason Tilan, and Joanna B. Kitlinska. "Abstract 3664: Hypoxia-induced phenotypic and metabolic changes in Ewing sarcoma cells trigger bone metastasis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3664.

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Zhu, Shiya, Akanksha Mahajan, Sung-Hyeok Hong, Susana Galli, Congyi Lu, You-Shin Chen, Sara Misiukiewicz, Stacey Chung, Jason Tilan, and Joanna B. Kitlinska. "Abstract 3664: Hypoxia-induced phenotypic and metabolic changes in Ewing sarcoma cells trigger bone metastasis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3664.

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Kieffer, N., M. Titeux, A. Henri, J. Breton-Gorius, and W. Vainchenker. "MEGAKARYOCYTIC ORIGIN OF PLATELET HLA CLASS I ANTIGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643546.

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The existence of HLA class I antigens on human platelets is well established. However, several authors have suggested that platelet HLA antigens are not integral membrane components but are acquired from soluble plasma sources and adsorbed to the platelet surface.In the present study, we used the monoclonal antibody W6/32, directed against a monomorphic epitope of the HLA class I antigen for the immunochemical characterization of platelet HLA. Immunoprecipitation experiments, performed after in vitro metabolic radiolabeling of human platelets revealed a band of molecular weight 44,000 identica

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Rapports d'organisations sur le sujet "Bone cells Metabolism"

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Leach, Roland M., Mark Pines, Carol V. Gay, and Shmuel Hurwitz. In vivo and in vitro Chondrocyte Metabolism in Relationship to the Developemnt of Tibial Dyschondroplasia in Broiler Chickens. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568090.bard.

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Skeletal deformities are a significant financial and welfare problem for the world poultry industry. Tibial dyschondroplasia (TD) is the most prevalent skeletal abnormality found in young broilers, turkeys and ducks. Tibial dyschondroplasia results from a perturbation of the sequence of events in the epiphyseal growth plate, the tissue responsible for longitudinal bone growth. The purpose of this investigation was to test the hypothesis that TD was the result of a failure of growth plate chondrocytes to differentiate and express the chemotactic molecules required for cartilage vascularization.

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Sela, Shlomo, and Michael McClelland. Desiccation Tolerance in Salmonella and its Implications. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7594389.bard.

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Salmonella enterica is a worldwide food-borne pathogen, which regularly causes large outbreaks of food poisoning. Recent outbreaks linked to consumption of contaminated foods with low water-activity, have raised interest in understanding the factors that control fitness of this pathogen to dry environment. Consequently, the general objective of this study was to extend our knowledge on desiccation tolerance and long-term persistence of Salmonella. We discovered that dehydrated STm entered into a viable-but-nonculturable state, and that addition of chloramphenicol reduced bacterial survival. Th

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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in esta

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