Bibliographies thématiques / Bone cells Metabolism

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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  1. Articles de revues
  2. Thèses
  3. Livres
  4. Chapitres de livres
  5. Actes de conférences
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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 et 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 (31 octobre 2016) : 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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3

Locci, P., E. Becchetti, G. Venti, C. Lilli, L. Marinucci, E. Donti, G. Paludetti et 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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4

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

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Motyl, Katherine J., Anyonya R. Guntur, Adriana Lelis Carvalho et Clifford J. Rosen. « Energy Metabolism of Bone ». Toxicologic Pathology 45, no 7 (octobre 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 interest in bone cell energetics because of the potential for these processes to be targeted for osteoporosis therapies. In contrast, due to the intimate link between bone and energy homeostasis, pharmaceuticals that treat metabolic disease or have metabolic side effects often have deleterious bone consequences. In this brief review, we will introduce osteoporosis, discuss how bone cells utilize energy to function, evidence for bone regulating whole body energy homeostasis, and some of the unanswered questions and opportunities for further research in the field.
6

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, et Gyula Poór. « Diabetes and bone metabolism ». Orvosi Hetilap 152, no 29 (juillet 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 controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions – PPARγ agonists – are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures. Orv. Hetil., 2011, 152, 1156–1160.
8

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

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9

Kim, Haemin, Brian Oh et Kyung-Hyun Park-Min. « Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism ». Cells 10, no 1 (7 janvier 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 increased risk of fracture. Targeting lipid metabolism with statin, a lipid-lowering drug, has been shown to improve bone density and quality in metabolic bone diseases. However, the molecular mechanisms of lipid-mediated regulation in osteoclasts are not completely understood. Thus, a better understanding of lipid metabolism in osteoclasts can be used to harness bone cell activity to treat pathological bone disorders. This review summarizes the recent developments of the contribution of lipid metabolism to the function and phenotype of osteoclasts.
10

Kim, Haemin, Brian Oh et Kyung-Hyun Park-Min. « Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism ». Cells 10, no 1 (7 janvier 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 increased risk of fracture. Targeting lipid metabolism with statin, a lipid-lowering drug, has been shown to improve bone density and quality in metabolic bone diseases. However, the molecular mechanisms of lipid-mediated regulation in osteoclasts are not completely understood. Thus, a better understanding of lipid metabolism in osteoclasts can be used to harness bone cell activity to treat pathological bone disorders. This review summarizes the recent developments of the contribution of lipid metabolism to the function and phenotype of osteoclasts.
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Articles de revues Thèses Livres

Thèses sur le sujet "Bone cells Metabolism":

1

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.
Title from document title page. Document formatted into pages; contains vi, 123 p. : ill. Includes abstract. Includes bibliographical references (p. 110-123).
3

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 studies where 1,25(OH)2D anticancer properties were assessed and initial findings that showed a requirement of other factors beyond VDR to induce 1,25(OH)2D signaling led to the identification of the retinoid X receptor, a common heterodimeric partner for several hormone receptors. The focus of thesis was to further elucidate the structure-function relationship of both the vitamin D receptor and the retinoid X receptor. Additionally, contributions to work directed towards further identifying the effects of vitamin D on osteoblast differentiation and survival. Interactions of 1,25(OH) 2D3 with its cognate receptor, identifying a key amino acid (Tryptophan 286) required for ligand contact and transcriptional activation, are described in Chapter 2. Mechanisms of vitamin D action on mesenchymal stem cell differentiation, promotion of osteoblast induction and maturation, and inhibition of adipocyte differentiation, are eluicidated in Chapter 3. Chapter 4 illustrates the effects of RAS/RAF/Mitogen-activated protein kinase mediated RXRalpha phosphorylation on the three-dimensional structure of the RXR/nuclear receptor partner heterodimers. Furthermore, this chapter reveals the inhibitory effect of the phosphorylation of a critical amino acid (serine 260) on the interaction of the AF-2 domain of the RXR with several coactivators, resulting in a decrease in the signaling potential of multiple steroid hormone receptors. The findings of this thesis further the knowledge of several areas of vitamin D biology, including both the canonical areas of bone formation, and the non-canonical area of vitamin D and cancer.
4

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.
Recently mutations in the bone morphogenic protein receptor type II (BMPRII) have been linked to the disease. Interestingly mutations in activin-like kinase-1 (ALK-1) and endoglin have been linked to hereditary haemorrhagic telangiectasia (HHT), a disease that results in PAH clinically indistinguishable from IPAH. All of these proteins are either receptors or co-receptors to members of the TGFbeta superfamily. The connection of these mutations to the disease still remains largely a mystery to researchers and the effects of either bone morphogenic proteins 2, 4, 7 or TGFbeta levels on endothelin-1(ET-1) production in human microvascular endothelial cells cultured from normal lungs (HMVEC-LBI) are unknown.
Methods: HMVEC-LBI cells were cultured in the presence of various concentrations of BMP 2,4,7 and TGFbeta, in complete media or serum starved conditions. After allotted time points the media was collected and assayed by ELISA, meanwhile the cells were lysed and protein content assayed for normalization purposes. Small Mothers against Decapentaplegic (SMAD) 1/5 phosphorylation was also measured.
Results and Conclusions: Despite evidence that all BMPs used were biologically active, namely through SMAD phosphorylation studies, only BMP7 at very high dosages increased ET-1 production levels. TGFbeta had a more pronounced effect at earlier time points with lower concentrations. The results provide insights on the effects of an important group of proteins, the BMPs and TGFbeta, on lung microvascular ECs and which are likely the key cellular player In IPAH development. These findings may have clinical relevance in terms of control of the disease and understanding the normal response of these cells BMPs and TGFbeta.
5

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.
"August 2004" Errata inside front cover. Bibliography: leaves 126-159.
7

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
8

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.
9

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 unique in its activation and function,making it relevant to understand how activation of each type of immune cell is regulated. Herewe describe the role of the nBMP2 protein in macrophage activation and function and the role ofthe CD5 co-receptor in helper T cell activation and function.The nuclear bone morphogenetic protein 2 (nBMP2) is the nuclear variant of the bonemorphogenetic protein 2 (BMP2), a growth factor important in heart development, neurogenesis,bone, cartilage and muscle development. To better understand the function of nBMP2, transgenicnBMP2 mutant mice were generated. These mice have a slow muscle relaxation and cognitivedeficit caused in part by abnormal Ca2+ mobilization. Mutant nBMP2 mice also have an impairedsecondary immune response to systemic bacterial challenge. Here we have further characterizedmacrophage activation and function from mutant nBMP2 mice before and after bacterialinfection. We describe how nBMP2 influences the Ca2+ mobilization response and phagocytosisin macrophages, revealing a novel role of the nBMP2 protein in immune cell regulation.CD5 is a surface marker on T cells, thymocytes, and the B1 subset of B cells. CD5 isknown to play an important role during thymic development of T cells. CD5 functions as anegative regulator of T cell receptor (TCR) signaling and fine tunes the TCR signaling response.Here we describe our characterization of CD5 regulation of Ca2+ signaling in naïve helper Tcells. We also outline our findings examining how CD5-induced changes in helper T cellactivation influence other biological processes such as immune cell metabolism, the diversity ofthe gut microbiome, and cognitive function and behavior. Thus, this work elucidates theinfluence of the CD5 co-receptor on the functional outcomes in multiple systems when CD5 isaltered.
10

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":

1

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

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2

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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3

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 condition is called haemolytic anaemia. The underlying defect is a deficiency in the activity of the enzyme glucose-6-phosphate dehydrogenase, termed G6PD deficiency.
4

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Sous la direction de 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)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
5

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 dysostoses tend to affect single bones or groups of bones, reflecting the transient nature of the many different signalling factors to which they are responsive during development. Abnormalities of bone density (high or low) may be due to primary deficiency of bone matrix synthesis (e.g. osteogenesis imperfecta and hypophosphatasia) but may also reflect an imbalance between bone formation and resorption. This may be caused by abnormalities of bone formation (e.g. hyperostosis/sclerosteosis and osteoporosis pseudoglioma syndrome) or bone resorption (e.g. classic osteopetrosis and fibrous dysplasia).
6

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 are a tissue that even in adult life retains the ability to change shape and structure depending on changes in their mechanical and hormonal environment, as well as self-renewal and repair capabilities. This process is called bone turnover. The basic processes of bone turnover are: • bone modeling (incessantly changes in bone shape during individual growth) following resorption and tissue formation at various locations (e.g. bone marrow formation) to increase mass and skeletal morphology. This process occurs in the bones of growing individuals and stops after reaching puberty • bone remodeling (processes involve in maintaining bone tissue by resorbing and replacing old bone tissue with new tissue in the same place, e.g. repairing micro fractures). It is a process involving the removal and internal remodeling of existing bone and is responsible for maintaining tissue mass and architecture of mature bones. Bone turnover is regulated by two types of transformation: • osteoclastogenesis, i.e. formation of cells responsible for bone resorption • osteoblastogenesis, i.e. formation of cells responsible for bone formation (bone matrix synthesis and mineralization) Bone maturity can be defined as the completion of basic structural development and mineralization leading to maximum mass and optimal mechanical strength. The highest rate of increase in pig bone mass is observed in the first twelve weeks after birth. This period of growth is considered crucial for optimizing the growth of the skeleton of pigs, because the degree of bone mineralization in later life stages (adulthood) depends largely on the amount of bone minerals accumulated in the early stages of their growth. The development of the technique allows to determine the condition of the skeletal system (or individual bones) in living animals by methods used in human medicine, or after their slaughter. For in vivo determination of bone properties, Abstract 10 double energy X-ray absorptiometry or computed tomography scanning techniques are used. Both methods allow the quantification of mineral content and bone mineral density. The most important property from a practical point of view is the bone’s bending strength, which is directly determined by the maximum bending force. The most important factors affecting bone strength are: • age (growth period), • gender and the associated hormonal balance, • genotype and modification of genes responsible for bone growth • chemical composition of the body (protein and fat content, and the proportion between these components), • physical activity and related bone load, • nutritional factors: – protein intake influencing synthesis of organic matrix of bone, – content of minerals in the feed (CA, P, Zn, Ca/P, Mg, Mn, Na, Cl, K, Cu ratio) influencing synthesis of the inorganic matrix of bone, – mineral/protein ratio in the diet (Ca/protein, P/protein, Zn/protein) – feed energy concentration, – energy source (content of saturated fatty acids - SFA, content of polyun saturated fatty acids - PUFA, in particular ALA, EPA, DPA, DHA), – feed additives, in particular: enzymes (e.g. phytase releasing of minerals bounded in phytin complexes), probiotics and prebiotics (e.g. inulin improving the function of the digestive tract by increasing absorption of nutrients), – vitamin content that regulate metabolism and biochemical changes occurring in bone tissue (e.g. vitamin D3, B6, C and K). This study was based on the results of research experiments from available literature, and studies on growing pigs carried out at the Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences. The tests were performed in total on 300 pigs of Duroc, Pietrain, Puławska breeds, line 990 and hybrids (Great White × Duroc, Great White × Landrace), PIC pigs, slaughtered at different body weight during the growth period from 15 to 130 kg. Bones for biomechanical tests were collected after slaughter from each pig. Their length, mass and volume were determined. Based on these measurements, the specific weight (density, g/cm3) was calculated. Then each bone was cut in the middle of the shaft and the outer and inner diameters were measured both horizontally and vertically. Based on these measurements, the following indicators were calculated: • cortical thickness, • cortical surface, • cortical index. Abstract 11 Bone strength was tested by a three-point bending test. The obtained data enabled the determination of: • bending force (the magnitude of the maximum force at which disintegration and disruption of bone structure occurs), • strength (the amount of maximum force needed to break/crack of bone), • stiffness (quotient of the force acting on the bone and the amount of displacement occurring under the influence of this force). Investigation of changes in physical and biomechanical features of bones during growth was performed on pigs of the synthetic 990 line growing from 15 to 130 kg body weight. The animals were slaughtered successively at a body weight of 15, 30, 40, 50, 70, 90, 110 and 130 kg. After slaughter, the following bones were separated from the right half-carcass: humerus, 3rd and 4th metatarsal bone, femur, tibia and fibula as well as 3rd and 4th metatarsal bone. The features of bones were determined using methods described in the methodology. Describing bone growth with the Gompertz equation, it was found that the earliest slowdown of bone growth curve was observed for metacarpal and metatarsal bones. This means that these bones matured the most quickly. The established data also indicate that the rib is the slowest maturing bone. The femur, humerus, tibia and fibula were between the values of these features for the metatarsal, metacarpal and rib bones. The rate of increase in bone mass and length differed significantly between the examined bones, but in all cases it was lower (coefficient b <1) than the growth rate of the whole body of the animal. The fastest growth rate was estimated for the rib mass (coefficient b = 0.93). Among the long bones, the humerus (coefficient b = 0.81) was characterized by the fastest rate of weight gain, however femur the smallest (coefficient b = 0.71). The lowest rate of bone mass increase was observed in the foot bones, with the metacarpal bones having a slightly higher value of coefficient b than the metatarsal bones (0.67 vs 0.62). The third bone had a lower growth rate than the fourth bone, regardless of whether they were metatarsal or metacarpal. The value of the bending force increased as the animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. The rate of change in the value of this indicator increased at a similar rate as the body weight changes of the animals in the case of the fibula and the fourth metacarpal bone (b value = 0.98), and more slowly in the case of the metatarsal bone, the third metacarpal bone, and the tibia bone (values of the b ratio 0.81–0.85), and the slowest femur, humerus and rib (value of b = 0.60–0.66). Bone stiffness increased as animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. Abstract 12 The rate of change in the value of this indicator changed at a faster rate than the increase in weight of pigs in the case of metacarpal and metatarsal bones (coefficient b = 1.01–1.22), slightly slower in the case of fibula (coefficient b = 0.92), definitely slower in the case of the tibia (b = 0.73), ribs (b = 0.66), femur (b = 0.59) and humerus (b = 0.50). Bone strength increased as animals grew. Regardless of the growth point tested, bone strength was as follows femur > tibia > humerus > 4 metacarpal> 3 metacarpal> 3 metatarsal > 4 metatarsal > rib> fibula. The rate of increase in strength of all examined bones was greater than the rate of weight gain of pigs (value of the coefficient b = 2.04–3.26). As the animals grew, the bone density increased. However, the growth rate of this indicator for the majority of bones was slower than the rate of weight gain (the value of the coefficient b ranged from 0.37 – humerus to 0.84 – fibula). The exception was the rib, whose density increased at a similar pace increasing the body weight of animals (value of the coefficient b = 0.97). The study on the influence of the breed and the feeding intensity on bone characteristics (physical and biomechanical) was performed on pigs of the breeds Duroc, Pietrain, and synthetic 990 during a growth period of 15 to 70 kg body weight. Animals were fed ad libitum or dosed system. After slaughter at a body weight of 70 kg, three bones were taken from the right half-carcass: femur, three metatarsal, and three metacarpal and subjected to the determinations described in the methodology. The weight of bones of animals fed aa libitum was significantly lower than in pigs fed restrictively All bones of Duroc breed were significantly heavier and longer than Pietrain and 990 pig bones. The average values of bending force for the examined bones took the following order: III metatarsal bone (63.5 kg) <III metacarpal bone (77.9 kg) <femur (271.5 kg). The feeding system and breed of pigs had no significant effect on the value of this indicator. The average values of the bones strength took the following order: III metatarsal bone (92.6 kg) <III metacarpal (107.2 kg) <femur (353.1 kg). Feeding intensity and breed of animals had no significant effect on the value of this feature of the bones tested. The average bone density took the following order: femur (1.23 g/cm3) <III metatarsal bone (1.26 g/cm3) <III metacarpal bone (1.34 g / cm3). The density of bones of animals fed aa libitum was higher (P<0.01) than in animals fed with a dosing system. The density of examined bones within the breeds took the following order: Pietrain race> line 990> Duroc race. The differences between the “extreme” breeds were: 7.2% (III metatarsal bone), 8.3% (III metacarpal bone), 8.4% (femur). Abstract 13 The average bone stiffness took the following order: III metatarsal bone (35.1 kg/mm) <III metacarpus (41.5 kg/mm) <femur (60.5 kg/mm). This indicator did not differ between the groups of pigs fed at different intensity, except for the metacarpal bone, which was more stiffer in pigs fed aa libitum (P<0.05). The femur of animals fed ad libitum showed a tendency (P<0.09) to be more stiffer and a force of 4.5 kg required for its displacement by 1 mm. Breed differences in stiffness were found for the femur (P <0.05) and III metacarpal bone (P <0.05). For femur, the highest value of this indicator was found in Pietrain pigs (64.5 kg/mm), lower in pigs of 990 line (61.6 kg/mm) and the lowest in Duroc pigs (55.3 kg/mm). In turn, the 3rd metacarpal bone of Duroc and Pietrain pigs had similar stiffness (39.0 and 40.0 kg/mm respectively) and was smaller than that of line 990 pigs (45.4 kg/mm). The thickness of the cortical bone layer took the following order: III metatarsal bone (2.25 mm) <III metacarpal bone (2.41 mm) <femur (5.12 mm). The feeding system did not affect this indicator. Breed differences (P <0.05) for this trait were found only for the femur bone: Duroc (5.42 mm)> line 990 (5.13 mm)> Pietrain (4.81 mm). The cross sectional area of the examined bones was arranged in the following order: III metatarsal bone (84 mm2) <III metacarpal bone (90 mm2) <femur (286 mm2). The feeding system had no effect on the value of this bone trait, with the exception of the femur, which in animals fed the dosing system was 4.7% higher (P<0.05) than in pigs fed ad libitum. Breed differences (P<0.01) in the coross sectional area were found only in femur and III metatarsal bone. The value of this indicator was the highest in Duroc pigs, lower in 990 animals and the lowest in Pietrain pigs. The cortical index of individual bones was in the following order: III metatarsal bone (31.86) <III metacarpal bone (33.86) <femur (44.75). However, its value did not significantly depend on the intensity of feeding or the breed of pigs.
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Bower, Mark, Louise Robinson et 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 pathogenesis, epidemiology, and management of the commonest paraneoplastic endocrinopathies including hypercalcaemia, Cushing’s syndrome, the syndrome of inappropriate antidiuresis, non-islet cell tumour hypoglycaemia, enteropancreatic hormone syndromes, Carcinoid syndrome, phaeochromocytoma, gonadotrophin secretion syndromes, prolactin and oxytocin secretion, and paraneoplastic pyrexia. The chapter concludes with a brief discussion of the management of metabolic disease in the context of advanced malignancy including hyperglycaemia, thyroid dysfunction, metabolic bone disease, renal failure, liver failure, and lactic acidosis.
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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., dir. 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, et 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":

1

Pignolo, Robert J., et Moustapha Kassem. « Circulating Osteogenic Cells ». Dans 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 ». Dans 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 et Larent Baud. « Arachidonic Acid Metabolism During Interactions Between Glomerular and Bone Marrow-Derived Cells ». Dans 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, et Olivier Hérault. « In Vitro Analysis of Energy Metabolism in Bone-Marrow Mesenchymal Stromal Cells ». Dans 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) ». Dans 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 ». Dans 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 et 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 ». Dans 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 ». Dans 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 et Jude E. Uzonna. « Isolation and Preparation of Bone Marrow-Derived Immune Cells for Metabolic Analysis ». Dans 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, et Connie Weaver. « Improving Human Nutrition : A Critical Objective for Potassium Recommendations for Agricultural Crops ». Dans 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.

Actes de conférences sur le sujet "Bone cells Metabolism":

1

Zhou, Xiaozhou, John E. Novotny et Liyun Wang. « Modeling Fluorescence Recovery After Photobleaching in Cyclically Loaded Bone : Potential Application in Quantitatively Measuring Load-Induced Solute Flows ». Dans 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 the molecular sieving properties [3–5], the fundamental mechanisms of solute transport around osteocytes still remain poorly understood, and solute flows have not been quantified in vivo.
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Li, Xiang-Qin, Ke-Dong Song et Tian-Qing Liu. « Growth and Metabolism of Bone Marrow Mesenchymal Stem Cells within Collagen Scaffolds in a Novel Bioreactor ». Dans 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, et 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 ». Dans 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 extravascular fluid displacements. This biophysical phenomenon is referred to as load-induced interstitial or extravascular fluid flow. In order to establish the role of convective transport mechanisms for maintenance of healthy bone metabolism and to investigate the potential role of convective transport (via load-induced fluid flow) for processes associated with functional adaptation, we developed a theoretical osteon model based on finite element methods. A study designed to simulate short term transport (circa 1 second or half a gait cycle) in a single osteon corroborated the hypothesis that diffusion alone is insufficient for molecular transport between the blood supply and remotely lying bone cells. Simulations of long term transport (circa one day) showed that convection via load-induced flow can be expected to improve this transport significantly.
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Trucco, Matteo, Nino Rainsusso, Piti Techavichit, Ronald Bernardi, Ryan Shuck, Laura Satterfield, Wendy Allen-Rhoades, Larry Donehower, David Loeb et Jason Yustein. « Abstract A70 : Targeting pediatric bone sarcoma stem cell with metabolic inhibitors ». Dans 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 et X. Edward Guo. « Design of a Microfluidic System for 3D Culture of Osteocytes In Vitro ». Dans 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 vitro studies addressing mechano-signal transduction mechanisms in bone cells including osteoblasts, osteocytes, and osteoclasts [1–8].
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Penninger, Charles L., Neal M. Patel et Andrés Tovar. « A Novel HCA Framework for Simulating the Cellular Mechanisms of Bone Remodeling ». Dans 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, and mineral homeostasis. An improved understanding of this process is necessary to identify patients at risk of bone disease and to assess appropriate treatment protocols. High-fidelity computer models are needed to understand the complex interaction of all parameters involved in bone remodeling. The primary focus of this investigation is to present a new computational framework that utilizes mathematical rules to mechanistically model the cellular mechanisms involved in the bone remodeling process. The computational framework used in this research combines accepted biological principles, cellular-level rules in a cellular automaton framework, and finite-element analysis. This computational model is referred to as hybrid cellular automaton (HCA) model. The simulations obtained with the HCA model allow to predict time-dependent morphology variations at the tissue level as a result of biological changes at the cellular level.
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Horiguchi, Atsushi, et Toshihiko Shiraishi. « Study on a Cell Mechanosensing System by Measuring Structural Deformation and Biochemical Response ». Dans 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 intracellular calcium ion concentration as biochemical response in a living cell stimulated by a micropipette. Gene transfection of green fluorescent protein to osteoblastic cells enabled visualization of actin in cells. When local deformation was applied to a single osteoblastic cell by a micropipette, the displacement distribution of cytoskeletal structure in the whole cell was automatically obtained from the two images of the cell before and after deformation by using Kanade-Lucas-Tomasi (KLT) method. Intracellular calcium ion response to mechanical stimulation was measured as the spatial and temporal changes of intensity of Fura Red loaded to a cell. As a result, we obtained the quantitative relationship between structural deformation and biochemical response of a cell and found that the change of calcium ion concentration increases with increasing the displacement of actin cytoskeleton. It indicates that the deformation of actin cytoskeleton is highly related to the cell mechanosensing system.
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Zhu, Shiya, Akanksha Mahajan, Sung-Hyeok Hong, Susana Galli, Congyi Lu, You-Shin Chen, Sara Misiukiewicz, Stacey Chung, Jason Tilan et Joanna B. Kitlinska. « Abstract 3664 : Hypoxia-induced phenotypic and metabolic changes in Ewing sarcoma cells trigger bone metastasis ». Dans 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 et Joanna B. Kitlinska. « Abstract 3664 : Hypoxia-induced phenotypic and metabolic changes in Ewing sarcoma cells trigger bone metastasis ». Dans 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 et W. Vainchenker. « MEGAKARYOCYTIC ORIGIN OF PLATELET HLA CLASS I ANTIGEN ». Dans 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 identical to that precipitated from metabolic labeled U937 or HEL cells. When the same antibody was tested by indirected immunofluorescence in a double labeling technique on in vitro cultures of human megakaryocytes, performed in the absence of human serum in the culture medium, megakaryocytes identified by an anti-vWF MoAb revealed a membrane staining with W6/32 identical to that observed on other bone marrow cells, e.g. macrophages. Our results provide evidence that platelet HLA has a megaka-ryocytic origin and that residual biosynthesis of HLA antigen does still occur in circulating platelets. However, our results do not exclude the ability of human platelets to adsord circulating HLA class I antigen from plasma.

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

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Leach, Roland M., Mark Pines, Carol V. Gay et 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, juillet 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. In this investigation in situ hybridization and immunocytochemical techniques were used to study chondrocyte gene products associated with cartilage maturation and vascularization such as osteopontin, osteonectin, type X collagen, and alkaline phosphatase. All markers were present in the growth plate tissue anter or to the TD lesion but were greatly diminished in the TD lesion. Thus, rather than not acquiring the markers for hypertrophy, it appears that the growth plate chondrocytes reach a certain stage of hypertrophy and then de-differentiate into cells which resemble chondrocytes in the prehypertrophic zone. Similar patterns were observed in all TD tissues examined whether the lesions were spontaneous or induced by dietary treatments or genetic selection. The decrease in gene expression can at least be partially explained by the fact that many of the dysplastic chondrocytes show classic signs of apoptosis. These results provide an explanation for the observation that a variety of genes show reduced expression in the TD lesion when examined by in situ hybridization. This would suggest that future research should focus on the earliest detectable stages in the development of TD and examine endocrine and autocrine factors which cause chondrocytes to de-differentiate and undergo premature apoptosis.
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Sela, Shlomo, et Michael McClelland. Desiccation Tolerance in Salmonella and its Implications. United States Department of Agriculture, mai 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. This finding implied that adaptation to desiccation stress requires de-novo protein synthesis. We also discovered that dried STm cells develop cross-tolerance to multiple stresses that the pathogen might encounter in the agriculture/food environment, such as high or low temperatures, salt, and various disinfectants. These findings have important implications for food safety because they demonstrate the limitations of chemical and physical treatments currently utilized by the food industry to completely inactivate Salmonella. In order to identify genes involved in desiccation stress tolerance, we employed transcriptomic analysis of dehydrated and wet cells and direct screening of knock-out mutant and transposon libraries. Transcriptomic analysis revealed that dehydration induced expression of ninety genes and down-regulated seven. Ribosomal structural genes represented the most abundant functional group with a relatively higher transcription during dehydration. Other large classes of induced functional groups included genes involved in amino acid metabolism, energy production, ion transport, transcription, and stress response. Initial genetic analysis of a number of up-regulated genes was carried out). It was found that mutations in rpoS, yahO, aceA, nifU, rpoE, ddg,fnr and kdpE significantly compromised desiccation tolerance, supporting their role in desiccation stress response.
3

Splitter, Gary A., Menachem Banai et Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, janvier 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 establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.

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