Relevant bibliographies by topics / Bone cells

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Bone cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Bone cells"

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Ahmed Elkammar, Hala. "Effect of human bone marrow derived mesenchymal stem cells on squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 110–16. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.14.

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Zahran, Faten, Ahmed Abdel Zaher Ahmed Abdel.Zaher, Nermin Raafat, and Mohamed Ali Mohamed Ali. "Hepatocyte derived from Rat Bone Marrow Mesenchymal Stem Cells." Indian Journal of Applied Research 3, no. 10 (October 1, 2011): 1–5. http://dx.doi.org/10.15373/2249555x/oct2013/135.

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RemyaV, RemyaV, Naveen Kumar, and Kutty M. V. H. Kutty M.V.H. "A Method for Cell Culture and RNA Extraction of Rabbit Bone Marrow Derived Mesenchymal Stem Cells." International Journal of Scientific Research 3, no. 7 (June 1, 2012): 31–33. http://dx.doi.org/10.15373/22778179/july2014/11.

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Van Epps, Heather L. "Bone cells unite." Journal of Experimental Medicine 202, no. 3 (August 1, 2005): 335. http://dx.doi.org/10.1084/jem2023iti3.

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Aubin, Jane E. "Bone stem cells." Journal of Cellular Biochemistry 72, S30-31 (1998): 73–82. http://dx.doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<73::aid-jcb11>3.0.co;2-l.

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Hashimoto, Futoshi, Kikuya Sugiura, Kyoichi Inoue, and Susumu Ikehara. "Major Histocompatibility Complex Restriction Between Hematopoietic Stem Cells and Stromal Cells In Vivo." Blood 89, no. 1 (January 1, 1997): 49–54. http://dx.doi.org/10.1182/blood.v89.1.49.

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Abstract Graft failure is a mortal complication in allogeneic bone marrow transplantation (BMT); T cells and natural killer cells are responsible for graft rejection. However, we have recently demonstrated that the recruitment of donor-derived stromal cells prevents graft failure in allogeneic BMT. This finding prompted us to examine whether a major histocompatibility complex (MHC) restriction exists between hematopoietic stem cells (HSCs) and stromal cells. We transplanted bone marrow cells (BMCs) and bones obtained from various mouse strains and analyzed the cells that accumulated in the engrafted bones. Statistically significant cell accumulation was found in the engrafted bone, which had the same H-2 phenotype as that of the BMCs, whereas only few cells were detected in the engrafted bones of the third-party H-2 phenotypes during the 4 to 6 weeks after BMT. Moreover, the BMCs obtained from the MHC-compatible bone showed significant numbers of both colony-forming units in culture (CFU-C) and spleen colony-forming units (CFU-S). These findings strongly suggest that an MHC restriction exists between HSCs and stromal cells.
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Hashimoto, Futoshi, Kikuya Sugiura, Kyoichi Inoue, and Susumu Ikehara. "Major Histocompatibility Complex Restriction Between Hematopoietic Stem Cells and Stromal Cells In Vivo." Blood 89, no. 1 (January 1, 1997): 49–54. http://dx.doi.org/10.1182/blood.v89.1.49.49_49_54.

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Graft failure is a mortal complication in allogeneic bone marrow transplantation (BMT); T cells and natural killer cells are responsible for graft rejection. However, we have recently demonstrated that the recruitment of donor-derived stromal cells prevents graft failure in allogeneic BMT. This finding prompted us to examine whether a major histocompatibility complex (MHC) restriction exists between hematopoietic stem cells (HSCs) and stromal cells. We transplanted bone marrow cells (BMCs) and bones obtained from various mouse strains and analyzed the cells that accumulated in the engrafted bones. Statistically significant cell accumulation was found in the engrafted bone, which had the same H-2 phenotype as that of the BMCs, whereas only few cells were detected in the engrafted bones of the third-party H-2 phenotypes during the 4 to 6 weeks after BMT. Moreover, the BMCs obtained from the MHC-compatible bone showed significant numbers of both colony-forming units in culture (CFU-C) and spleen colony-forming units (CFU-S). These findings strongly suggest that an MHC restriction exists between HSCs and stromal cells.
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Chambers, T. J., and K. Fuller. "Bone cells predispose bone surfaces to resorption by exposure of mineral to osteoclastic contact." Journal of Cell Science 76, no. 1 (June 1, 1985): 155–65. http://dx.doi.org/10.1242/jcs.76.1.155.

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The cell-free endocranial surface of young adult rat parietal bones was used as a substrate for osteoclastic bone resorption, either without prior treatment, or after incubation of the parietal bones with collagenase or neonatal rat calvarial cells. Untreated, the endocranial surface consisted of unmineralized organic fibres; incubation with calvarial cells or collagenase caused disruption and removal of these fibres, with extensive exposure of bone mineral on the endocranial surface, without morphologically detectable mineral dissolution. Neonatal rabbit osteoclasts resorbed bone to a greater extent from parietal bones pre-incubated with calvarial cells or collagenase than from untreated bones; mineral exposure and subsequent osteoclastic resorption were both increased if calvarial cells were incubated with parathyroid hormone; removal of bone mineral after incubation with calvarial cells removed the predisposition to osteoclastic resorption. These experiments demonstrate that calvarial cells are capable of osteoid destruction, and indicate that one mechanism by which osteoblasts induce osteoclastic bone resorption may be through digestion of the unmineralized organic material that covers bone surfaces, to expose the underlying resorption-stimulating bone mineral to osteoclastic contact.
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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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Kelder, Cindy, Cornelis J. Kleverlaan, Marjolijn Gilijamse, Astrid D. Bakker, and Teun J. de Vries. "Cells Derived from Human Long Bone Appear More Differentiated and More Actively Stimulate Osteoclastogenesis Compared to Alveolar Bone-Derived Cells." International Journal of Molecular Sciences 21, no. 14 (July 17, 2020): 5072. http://dx.doi.org/10.3390/ijms21145072.

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Osteoblasts derived from mouse skulls have increased osteoclastogenic potential compared to long bone osteoblasts when stimulated with 1,25(OH)2 vitamin D3 (vitD3). This indicates that bone cells from specific sites can react differently to biochemical signals, e.g., during inflammation or as emitted by bioactive bone tissue-engineering constructs. Given the high turn-over of alveolar bone, we hypothesized that human alveolar bone-derived osteoblasts have an increased osteogenic and osteoclastogenic potential compared to the osteoblasts derived from long bone. The osteogenic and osteoclastogenic capacity of alveolar bone cells and long bone cells were assessed in the presence and absence of osteotropic agent vitD3. Both cell types were studied in osteogenesis experiments, using an osteogenic medium, and in osteoclastogenesis experiments by co-culturing osteoblasts with peripheral blood mononuclear cells (PBMCs). Both osteogenic and osteoclastic markers were measured. At day 0, long bones seem to have a more late-osteoblastic/preosteocyte-like phenotype compared to the alveolar bone cells as shown by slower proliferation, the higher expression of the matrix molecule Osteopontin (OPN) and the osteocyte-enriched cytoskeletal component Actin alpha 1 (ACTA1). This phenotype was maintained during the osteogenesis assays, where long bone-derived cells still expressed more OPN and ACTA1. Under co-culture conditions with PBMCs, long bone cells also had a higher Tumor necrose factor-alfa (TNF-α) expression and induced the formation of osteoclasts more than alveolar bone cells. Correspondingly, the expression of osteoclast genes dendritic cell specific transmembrane protein (DC-STAMP) and Receptor activator of nuclear factor kappa-Β ligand (RankL) was higher in long bone co-cultures. Together, our results indicate that long bone-derived osteoblasts are more active in bone-remodeling processes, especially in osteoclastogenesis, than alveolar bone-derived cells. This indicates that tissue-engineering solutions need to be specifically designed for the site of application, such as defects in long bones vs. the regeneration of alveolar bone after severe periodontitis.
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Dissertations / Theses on the topic "Bone cells"

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Fong, Jenna. "Breast cancer cells affect bone cell differentiation and the bone microenvironment." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104758.

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Breast carcinoma is the most commonly diagnosed cancer among women worldwide, with approximately 1 in 7 expected to be affected during her lifetime. The spread of breast cancer to secondary sites is generally incurable. Bone is the preferred site of metastasis, where the development of a secondary tumour causes severe osteolysis, hypercalcemia and a considerable pain burden. However, how breast cancer cells establish supportive interactions with bone cells is not well understood. We have examined the effects of factors released from MDA-MB-231 and 4T1 breast cancer cells on the differentiation of C57BL6 mouse bone marrow cells. Treatment with cancer-derived factors resulted in a sustained 40–60% decrease in osteoblast differentiation markers, and induced an osteoclastogenic change in the ratio of receptor activator of NF-κB ligand (RANKL) to osteoprotegerin (OPG). Importantly, exposure of bone cells to breast cancer-derived factors stimulated the subsequent attachment of cancer cells to immature osteoblasts. Inhibition of γ-secretase using pharmacological inhibitors DAPT and Compound E completely reversed cancer-induced osteoclastogenesis as well as cancer-induced enhancement of cancer cell attachment, identifying γ-secretase activity as a key mediator of these effects. We next evaluated the effects of breast cancer cells on the energy metabolism of bone cells. Treatment of bone marrow cells with conditioned medium from 4T1 breast cancer cells resulted in an increase in glucose consumption by bone cells, higher mitochondrial transmembrane potential, and a 2.3-fold rise in cellular ATP content. In addition, breast cancer derived factors stimulated the expression of mRNA and protein levels of metabolic sensor, AMP-regulated protein kinase (AMPK). To assess if such change in cell bioenergetics may have consequences for cell differentiation and activity, we used defined models of osteoclastogenesis, and increased precursor metabolic activity by providing excess energy substrates. We have found that an increase in mitochondrial transmembrane potential and cellular ATP levels during osteoclastogenesis resulted in the formation of larger osteoclasts that demonstrate higher resorptive activity. Thus, we have uncovered that osteoblasts act as a critical intermediate of premetastatic signalling by breast cancer cells, and pinpointed γ-secretase as a robust target for developing therapeutics potentially capable of reducing both the homing and progression of cancer metastases to bone. In addition, we have discovered heightened energetics in bone cells exposed to breast cancer cell-released factors, which may contribute to the formation of larger, more active osteoclasts. Modification of the AMPK pathway may prove an important therapeutic target for breast cancer metastasis to bone.
Le cancer du sein est le cancer plus diagnostiqué chez les femmes. On estime qu'environ une femme sur sept en sera affectée. La diffusion du cancer du sein aux emplacements secondaires est généralement incurable. L'os est l'emplacement préféré de la métastase, où le développement d'une tumeur secondaire cause de l'osteolyse, de l'hypercalcemie, et une douleur considérable. Cependant, comment les cellules de cancer du sein établissent des interactions supportifs avec des cellules d'os n'est pas bien compris. Nous avons examiné les effets des facteurs libérés des cellules du cancer du sein MDA-MB-231 et 4T1 sur la différentiation des cellules de moelle de la souris C57BL6. Le traitement avec des facteurs cancer-dérivés a produit une diminution de 40-60% des marqueurs de différentiation d'osteoblast, comparé au traitement par l'acide ascorbique, et a induit un changement osteoclastogenique dans le rapport du RANKL/osteoprotegerin. L'exposition des cellules d'os à des facteurs dérivés du cancer du sein a ensuite stimulé l'attachement des cellules cancéreuses aux osteoblasts non mûrs. L'inhibition du γ-secretase utilisant les inhibiteurs pharmacologiques DAPT et le Compound E a complètement inversé l'osteoclastogenise cancer-induit aussi bien que le perfectionnement cancer-induit de l'attachement de cellules cancéreuses, identifiant l'activité de le γ-secretase comme étant le médiateur principal de ces effets. Nous avons ensuite évalué les effets des cellules cancereuse sur le métabolisme énergétique des cellules d'os. Le traitement des cellules de moelle avec le medium conditionné des cellules du cancer du sein 4T1 a eu comme conséquence une augmentation des mitochondries à haut-potentiel de membrane, une augmentation de 2.3 fois le contenu cellulaire de triphosphate d'adénosine, et une consommation plus rapide du glucose. Ce changement de l'énergétique a été accompagné d'une stimulation d'AMPK dans la protéine et l'ADN messagère. Pour évaluer les effets du statut de haute énergie dans les osteoclasts, nous avons élevé l'énergique des osteoclasts avec du pyruvate de sodium. Cette addition a causée une croissance des osteoclasts, avec des plus grands nucleus, et la résorption de plus de substrat. Ainsi, nous avons découvert l'osteoblast comme étant un intermédiaire clé à la signalisation prémetastatique par des cellules du cancer du sein. Nous avons aussi indiqué le γ-secretase comme cible robuste pour le developpement de thérapeutique potentiellement capable de réduire l'autoguidage et la progression des métastases de cancer à l'os. Additonellement, nous avons découvert l'énergétique intensifiée chez les cellules d'os exposées aux facteurs cellule-libérés par le cancer du sein, qui mène à une osteoclastogenesise plus active et plus importante. La modification de la voie d'AMPK peut s'avérer être une cible thérapeutique importante pour que la métastase de cancer du sein aux os.
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Hoebertz, Astrid. "Purinergic signalling in bone cells." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249706.

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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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Malone, Amanda Michelle Dolphin. "Mechanotransduction mechanisms in bone cells /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Porter, Ryan Michael. "Examination of Glucocorticoid Treatment on Bone Marrow Stroma: Implications for Bone Disease and Applied Bone Regeneration." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/36365.

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Long-term exposure to pharmacological doses of glucocorticoids has been associated with the development of osteopenia and avascular necrosis. Bone loss may be partially attributed to a steroid-induced decrease in the osteoblastic differentiation of multipotent progenitor cells found in the bone marrow. In order to determine if there is a change in the osteogenic potential of the bone marrow stroma following glucocorticoid treatment, Sprague-Dawley rats were administered methylprednisolone for up to six weeks, then sacrificed at 0, 2, 4, or 6 weeks during treatment or 4 weeks after cessation of treatment. Femurs were collected and analyzed for evidence of steroid-induced osteopenia and bone marrow adipogenesis. Although glucocorticoid treatment did inhibit bone growth, differences in ultimate shear stress and mineral content were not detected. The volume of marrow fat increased with increasing duration of treatment, but returned to near control levels after cessation of treatment. Marrow stromal cells were isolated from tibias, cultured in the presence of osteogenic supplements, and analyzed for their capacity to differentiate into osteoblast-like cells in vitro. Glucocorticoid treatment diminished the absolute number of isolated stromal cells, but did not inhibit the relative levels of bone-like mineral deposition or osteocalcin expression and secretion. Although pharmacological glucocorticoid levels induce bone loss in vivo, physiologically equivalent concentrations have been shown to enhance the formation of bone-like tissue in vitro. However, glucocorticoids have also been reported to inhibit proliferation and type I collagen synthesis in marrow stromal cell cultures. In order to assess the effects of intermittent dexamethasone treatment on the progression of osteogenesis in rat marrow stromal cell culture, this synthetic glucocorticoid was removed from the culture medium after a variable period of initial supplementation. Cell layers were analyzed for total cell number, collagen synthesis, phenotypic marker expression, and matrix mineralization. Prolonged supplementation with dexamethasone decreased proliferation, but did not significantly affect collagen synthesis. Furthermore, increased treatment duration was found to increase bone sialoprotein expression and mineral deposition. The duration of glucocorticoid treatment may be a key factor for controlling the extent of differentiation in vitro.
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Bennett, Jonathan Hilary. "The differentiation of osteogenic cells from bone marrow." Thesis, University of Oxford, 1991. http://ora.ox.ac.uk/objects/uuid:3460f26e-a124-4605-8601-2e300241de14.

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Gronthos, Stan. "Stromal precursor cells : purification and the development of bone tissue." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phg8757.pdf.

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Bibliography: leaves 152-223. Experiments were designed to identify and purify human bone marrow stromal precursor cells by positive immunoselection, based on the cell surface expression of the VCAM-1 and STRO-1 antigens. The data presented demonstrates a hierarchy of bone cell development in vitro.
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Kandimalla, Yugandhar. "Study of Chitosan Microparticles with Bone Marrow Mesenchymal Stem Cells for Bone Tissue Regeneration." University of Toledo Health Science Campus / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=mco1250778129.

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Wigzell, Cathy. "Differentiation of bone cells in vitro." Thesis, University of St Andrews, 1990. http://hdl.handle.net/10023/14070.

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Osteoblastic differentiation was studied in vitro using primary cultures of bone cells derived from neonatal mouse calvaria. Using alkaline phosphatase as a marker, maintenance of the osteoblastic phenotype was found to be dependent upon the presence of ascorbic acid. No toxic effect due to ascorbic acid was seen. Insulin and dexamethasone were found to stimulate alkaline phosphatase expression, the former only in the absence of ascorbic acid. Two growth factors, epidermal growth factor and platelet-derived growth factor, were found to inhibit alkaline phosphatase expression in the presence of ascorbic acid. Osteogenesis was most pronounced in cultures supplemented with ascorbic acid. The osteoblasts formed multilayers of cells and secreted an organic extracellular matrix composed mainly of type I collagen. Matrix vesicles were found among the collagen fibres. In the presence of 6-glycerophosphate, calcium phosphate crystals were deposited in discrete patches forming a mineralisation front which progressively engulfed osteoblasts. The type of matrix formed and the pattern of mineralisation resembled those of lamellar bone. Insulin at 5000ng/ml stimulated matrix calcification in the absence of ascorbic acid. Dexamethasone, EGF and PDGF inhibited calcification. The extent of calcification was dependent upon the concentration of glycerophosphate in the culture medium. Conditioned medium from osteogenic cultures contained a GM-CSF which was secreted constitutively by the osteoblasts. Preliminary experiments with a mesenchymal stem cell line, Balb/c 3T3, showed the existence of a factor(s) with mitogenic activity in bone cell conditioned medium. No inducer of osteogenic differentiation was found.
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Weber, Matthew Charles. "Engineering human bone marrow stromal cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1055867071.

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Books on the topic "Bone cells"

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Bone research protocols. 2nd ed. New York: Humana Press, 2012.

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A manual for differentiation of bone marrow-derived stem cells to specific cell types. New Jersey: World Scientific, 2014.

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Pathology of bone marrow and blood cells. 2nd ed. Baltimore, Md: Lippincott William & Wilkins, 2009.

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Thomas, Gethin Penar. Load responsiveness of bone marrow stromal cells. Birmingham: University of Birmingham, 1994.

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Preston, Michael Robert. Signal transducing ion channels of bone cells. Birmingham: University of Birmingham, 1997.

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Gu, Yuchun. Investigation of ion channels on bone cells. Birmingham: University of Birmingham, 2000.

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Diggs, L. W. The morphology of human blood cells. 6th ed. Abbott Park, Ill: Abbott Laboratories, 2003.

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International Workshop on Cells and Cytokines in Bone and Cartilage (2nd 1988 Davos, Switzerland). Second International Workshop on Cells and Cytokines in Bone and Cartilage: 9-12 April 1988, Davos, Switzerland : abstracts. New York, N.Y: Springer International, 1988.

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International, Workshop on Cells and Cytokines in Bone and Cartilage (3rd 1990 Davos Switzerland). Third International Workshop on Cells and Cytokines in Bone and Cartilage: 8-11 April 1990, Davos, Switzerland : abstracts. New York, N.Y: Springer International, 1990.

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Antin, Joseph H. Manual of stem cell and bone marrow transplantation. New York: Cambridge University Press, 2009.

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Book chapters on the topic "Bone cells"

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Oranger, Angela, Graziana Colaianni, and Maria Grano. "Bone Cells." In Imaging of Prosthetic Joints, 3–13. Milano: Springer Milan, 2014. http://dx.doi.org/10.1007/978-88-470-5483-7_1.

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Gooch, Keith J., and Christopher J. Tennant. "Bone Cells." In Mechanical Forces: Their Effects on Cells and Tissues, 55–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03420-0_3.

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Reza Rezaie, Hamid, Mohammad Hossein Esnaashary, Masoud Karfarma, and Andreas Öchsner. "Productivity: Cells." In Bone Cement, 43–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39716-6_3.

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Oni, Olusola O. A., S. Dearing, and S. Pringle. "Endothelial Cells and Bone Cells." In Bone Circulation and Vascularization in Normal and Pathological Conditions, 43–48. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2838-8_5.

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Nakano, Toru, Takumi Era, Hiroaki Kodama, and Tasuku Honjo. "Development of Blood Cells from Mouse Embryonic Stem Cells in Culture." In Bone Marrow Transplantation, 9–19. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_2.

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Gotfried, Y., J. Yaremchuk, M. A. Randolph, and A. J. Weiland. "The Target Cells in Vascularized Bone Allografts." In Bone Transplantation, 111–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83571-1_17.

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Boyce, B. F., D. E. Hughes, K. R. Wright, L. Xing, and A. Dai. "Apoptosis in Bone Cells." In Novel Approaches to Treatment of Osteoporosis, 61–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-09007-7_3.

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Barcellos-Hoff, Mary Helen. "Bone Marrow-derived Cells." In Encyclopedia of Systems Biology, 152–54. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1395.

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Duong, Minh Ngoc, Yu-Ting Ma, and Ray C. J. Chiu. "Bone Marrow Stem Cells." In Methods in Molecular Biology, 33–46. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-511-8_3.

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Ho, A. D., and W. Wagner. "Bone Marrow Niche and Leukemia." In Cancer Stem Cells, 125–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/2789_2007_048.

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Conference papers on the topic "Bone cells"

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Ominsky, Michael S., Philippe K. Zysset, and Steven A. Goldstein. "Elastic Properties of 3D Cells for Trabecular Bone: Digital vs. Structural Finite Element Models." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0201.

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Abstract Characterizing morphological and elastic properties of trabecular bone is a critical step towards understanding bone fragility. Idealized 3D cells for trabecular bone based on a tetrakaidecahedral geometry have been previously described to study morphology and its relationship to mechanical properties [1,2]. Two types of cells have been proposed: an open cell consisting of rectangular beams and a closed cell with hexagonal plates [Fig. 1]. The morphology of the cell is quantified by measures of structural density (SD) and mean intercept length (MIL). Structural density is mainly controlled by the aspect ratio t/l (thickness/length) of the beams or plates. Mean intercept length is controlled by the angle θ, which changes the cell’s anisotropy.
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Shikata, Tetsuo, Toshihiko Shiraishi, Kumiko Tanaka, Shin Morishita, and Ryohei Takeuchi. "Effects of Amplitude and Frequency of Vibration Stimulation on Cultured Osteoblasts." In ASME 2007 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/detc2007-34949.

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Mechanical stimulation to bones affects osteogenesis such as decrease of bone mass of astronauts under zero gravity, walking rehabilitation to bone fracture and fracture repair with ultrasound devices. Bone cells have been reported to sense and response to mechanical stimulation at cellular level morphologically and metabolically. In the view of mechanical vibrations, bone cells are deformed according to mechanical stimulation and their mechanical characteristics. Recently, it was reported that viscoelasticity of cells was measured using tensile and creep tests and that there was likely natural frequency and nonlinearity of cells in the sense of structural dynamics. It suggests that there is effective frequency and amplitude of mechanical stimulation on osteogenesis by bone cells. In this study, sinusoidal inertia force was applied to cultured osteoblasts, MC3T3-E1, and effects of frequency and acceleration amplitude of mechanical vibration on the cells were investigated in respect of cell proliferation, cell morphology, bone matrix generation and alkaline phosphatase (ALP) gene expression. After the cells were cultured in culture plates in a CO2 incubator for one day and adhered on the cultured plane, vibrating groups of the culture plates were set on an aluminum plate attached to a exciter and cultured under sinusoidal excitation in another incubator separated from non-vibrating groups of the culture plates. Acceleration amplitude and frequency were set to several kinds of conditions. The time evolution of cell density was obtained by counting the number of cells with a hemocytometer. The cell morphology was observed with a phase contrast microscope. Calcium salts generated by the cells were observed by being stained with alizarin red S solution and their images were captured with a CCD camera. The vibrating groups for the cell proliferation and the calcium salts staining were sinusoidally excited for 24 hours a day during 28-day cultivation. Gene expression of ALP was measured by a real-time RT-PCR method. After the vibrating groups for the PCR were excited for 6 hours, the total RNAs were extracted. After reverse transcription, real-time RT-PCR was performed. Gene expression for ALP and a housekeeping gene were determined simultaneously for each sample. Gene levels in each sample were normalized to the measured housekeeping gene levels. As a result, it is shown that saturate cell density becomes high and bone matrix generation is promoted by applying mechanical vibration and that there may be some peaks to frequency and a certain threshold value to acceleration amplitude of mechanical vibration for saturation cell density and bone matrix generation.
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Romito, Marilisa, Konstantina M. Stankovic, and Demetri Psaltis. "Imaging of cochlear cells through scattering bone." In Frontiers in Optics. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/fio.2018.jw3a.111.

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Ganji, Yasaman, and Mehran Kasra. "Comparison of Mechanosensitivity of Human Primary-Cultured Osteoblast Cells and Human Osteosarcoma Cell Line Under Hydrostatic Pressure." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80030.

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Regarding to the advances in mechanical stimulation of cells, this study aims to address important issues in bone generation and therapy at cellular level as it relates to understanding of bone cell response to hydrostatic pressure as well as choosing a proper cell model in studies of bone cell response to mechanical stimulation. G292 human osteosarcoma cell line and human primary osteoblast cells were tested under cyclic hydrostatic pressure. Monolayer culture of cells were divided into three groups of control without loading, static with the pressure of 0.5 MPa, and dynamic with the pressure of 0.5 MPa and the frequency of 1 Hz. The cells were analyzed with measurement of alkaline phosphatase activity. Higher level of alkaline phosphatase activity in all groups of primary cell model compared with cell line model indicated more sensitivity of response of primary cells to this kind of loading.
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Uddin, Sardar M. Zia, and Yi-Xian Qin. "Anabolic Effects of Ultrasound as Countermeasures of Simulated Microgravity in In-Vitro and In-Vivo Functional Disuse Models." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53796.

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Microgravity (MG) during space flight has been known to cause adverse effect on bone quality. Data collected from studies done on spaceflights show loss of 1–1.6% bone mineral density (BMD) per space-flight-month[1]. Most BMD has been recorded in load-bearing bones [2]. Some studies has considered using drugs and different growth factors to maintain bone mass in microgravity conditions but it can be too expensive to maintain over longer periods of time besides the systematic effects of such treatments [3]. Considering the effects of microgravity are partially attributed to lack of mechanical force on bone tissue, which alters gene expression, reduction in transcription factors and growth factors. Furthermore, lack of gravity effects cell growth, proliferation, differentiation, cytoskeleton polymerization and cellular morphology [4, 5]. Thus to reverse these adverse effects on bone physiology, it is important to provide cells with mechanical stimulus which can provide essential mechanical signal for cells to counter the effects of microgravity. Ultrasound acoustic vibrations can be readily applied in, in vivo and human studies and has shown anabolic effects on osteopenic bone tissue [6]. Furthermore, ultrasound is a non-invasive and more target specific treatment relative to cyclic strain and vibration. The objective of this study is to see effects of low intensity pulsed ultrasound (LIPUS) on disused bone model and osteogenic activity of osteoblast cells cultures in simulated microgravity. This will help us understand that effects of ultrasound on microgravity and mechanotransduction pathway responsible for anabolic effect on bone cells.
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Cowin, Stephen C. "The Search for Mechanism in Bone Adaptation Studies." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-1929.

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Abstract The mechanosensory mechanisms in bone include (i) the cell system that is stimulated by external mechanical loading applied to the bone; (ii) the system that transduces that mechanical loading to a communicable signal; and (iii) the systems that transmit that signal to the effector cells for the maintenance of bone homeostasis and for strain adaptation of the bone structure. The effector cells are the osteoblasts and the osteoclasts. These systems and the mechanisms that they employ have not yet been unambiguously identified. The candidate systems are reviewed here. The current theoretical and experimental evidence, which suggests that osteocytes are the principal mechanosensory cells of bone, is summarized. This evidence shows that they are activated by shear stress from fluid flowing through the osteocyte canaliculi. The evidence also suggests that the electrically coupled three-dimensional network of osteocytes and lining cells is a communications system for the control of bone homeostasis and structural strain adaptation.
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Lan, Sheeny K., Daniel N. Prater, Russell D. Jamison, David A. Ingram, Mervin C. Yoder, and Amy J. Wagoner Johnson. "Vasculogenic Potential of Porcine Endothelial Colony Forming Cells." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192848.

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The natural healing process cannot restore form and function to critical size bone defects without the presence of a graft to support and guide tissue regeneration [1]. Critical size bone defects in humans are typically on the order of centimeters or larger [2]. Thus, a major limitation of synthetic grafts or bone tissue engineering constructs is the lack of vascularization to support cell viability after placement in vivo [3]. Cells that participate in bone regeneration, must reside within 150–200 microns of a blood supply in order to gain proper nutrients and to eliminate waste [4]. Consequently, a tissue engineering construct of a clinically relevant size cannot rely on diffusion for transport of nutrients and waste. Previous research has shown that blood vessels can infiltrate scaffolds, but the overall process is too slow to prevent death of cells located in the center of a construct [5].
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Jeon, Jong Heon, Tae Kyung Kim, So Hee Park, Jung Wook Shin, and Ok Chan Jeong. "Experimental Study on Cytoplasmic Calcium Oscillation in MG-63 Cells Induced by Pressure-Driven Fluid Flow." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11121.

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This paper determined the optimal periodic mechanical stimulation of live bone cells from the intracellular calcium oscillation induced by shear stress. The shear stress-induced intracellular calcium responses of cells on a micro-cell chip were measured to study the mechanotransduction of bone cells. From the measured static and dynamic characteristics of the internal cellular signaling in cells, the optimum duration of the mechanical stimulation is determined.
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Srinivasan, Jayendran, Vincent Kish, Sydha Salihu, Madhavi Ayyalasomayajula, and Nilay Mukherjee. "Poking Cells in Cell-Gel Constructs: A Potential Way of Measuring Fluid Pressure in Cells." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61290.

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In this study, fluorescently labeled ATDC5 and bone marrow derived preosteoblastic cells were embedded in agarose gel and poked with a micropipette under a confocal microscope. Image stacks of cross sections of cells were taken before and after poking and the largest cross sectional areas were analyzed. After adjusting for photobleaching effects by equalizing the area of a nearby unpoked cell (by adjusting threshold values of the images) the area of the poked cell before and after poking was measured and the percentage change in area was calculated. The percentage change in cross sectional area was 25 ± 15% for ATDC5 cells and 31 ±13% for bone marrow derived cells (n= 5 for each type of cell). The decrease in area was statistically significant for each cell type (p&lt;0.05). There was no difference in the reduction in areas between the two types of cells (power &gt;80%). These results are consistent with the theory that some of the cell water is free and some are structured or restricted. This method can be utilized to determine fluid pressure in cells. This is significant because it is believed that changes in intracellular fluid pressure can play a role in cellular mechanotransduction.
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Millon, Debra Chenet, Darren L. Hitt, and Stephan J. LaPointe. "Heat Generation in Bone Cutting-Implications for Thermal Necrosis." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/htd-24430.

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Abstract A bunion is a common foot disorder caused by an abnormal outward projection of the joint and inward turning of the toe. Surgery to correct the malformation involves cutting the first metatarsal head, repositioning and setting it; the bone is then left to heal itself over time. A potentially serious by-product of the bone cutting is the frictional heat generated. While the heat susceptibility of individual bone cells varies throughout bone and is difficult to quantify, studies have shown that when injured, bone may not always heal as bone but rather as a fibrous tissue of varying degrees of differentiation. Prolonged heat exposure at or above critical temperatures may also lead to fat and bone cell resorption, a subsequent fat cell degeneration of the tissue, local swelling of cells as well as denaturation of the enzymatic and membrane proteins (Eriksson & Albrektsson, 1983, Li et al, 1999).
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Reports on the topic "Bone cells"

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Dooner, Mark, Jason M. Aliotta, Jeffrey Pimental, Gerri J. Dooner, Mehrdad Abedi, Gerald Colvin, Qin Liu, Heinz-Ulli Weier, Mark S. Dooner, and Peter J. Quesenberry. Cell Cycle Related Differentiation of Bone Marrow Cells into Lung Cells. Office of Scientific and Technical Information (OSTI), December 2007. http://dx.doi.org/10.2172/936517.

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Mastro, Andrea M. Trafficking of Metastatic Breast Cancer Cells in Bone. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada433936.

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Mastro, Andrea M. Trafficking of Metastatic Breast Cancer Cells in Bone. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada460748.

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Gay, Carol V. Directed Secretion by Bone Cells of a Factor that Attracts Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada398984.

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Park, Serk I. Activation of Myeloid-Derived Suppressor Cells in Bone Marrow. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada600504.

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Donohue, Henry J., Christopher Niyibizi, and Alayna Loiselle. Induced Pluripotent Stem Cell Derived Mesenchymal Stem Cells for Attenuating Age-Related Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada606237.

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Donahue, Henry J. Induced Pluripotent Stem Cell Derived Mesenchymal Stem Cells for Attenuating Age-Related Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada581680.

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Shevde-Samant, Lalita. Crosstalk Between Cancer Cells and Bones Via the Hedgehog Pathway Determines Bone Metastasis of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada487471.

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Donahue, Henry J. Fluid Flow Sensitivity of Bone Cells as a Function of Age. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada401057.

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Majeska, Robert J., and Mitchell B. Schaffler. Role of Bone Remodeling in Skeletal Colonization by Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada444893.

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