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Relevant bibliographies by topics / Osteoblast / Books

Books on the topic 'Osteoblast'

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Author: Grafiati

Published: 4 June 2021

Last updated: 14 March 2023

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1

Najafova, Zeynab. Epigenetic regulation of osteoblast differentiation. Göttingen: Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017.

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2

Knight, Susan Mary. A study of osteoblast function in osteoporosis. Birmingham: University of Birmingham, 1994.

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3

Tarrant, Sarah Fiona. Osteoblast interactions with bone biomaterials 'in vitro'. Birmingham: Universityof Birmingham, 1989.

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4

Liu, Fina. Molecular and cellular analysis of the osteoblast lineage. [Toronto: University of Toronto, Faculty of Dentistry], 1997.

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5

Al-Ajmi, Nada Mohammad Zaid. The effect of clinostat rotation on osteoblast behaviour. Manchester: University of Manchester, 1997.

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6

Horgan, Fergal G. Osteoblast response to sputter deposited calcium phosphate thin film coatings. [S.l: The author], 2004.

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7

Steven, Doty, and United States. National Aeronautics and Space Administration., eds. Effects of hypogravity on osteoblast differentiation: Final report, NCC 2-846. [Washington, DC: National Aeronautics and Space Administration, 1997.

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8

Perry, Judith Louise. Production and characterisation of monoclonal antibodies to rat osteoblast-like cells. Birmingham: University of Birmingham, 1989.

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9

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

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10

Turksen, Kursad. Analysis of the osteoblast lineage: Use of a cell culture model and monoclonal antibodies. [S.l.]: K. Turksen, 1991.

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11

Siegert, Peter. Pasteurella multocida toxin prevents osteoblast differentiation by transactivation of the MAP-kinase cascade via the Gaq/11 - p63RhoGEF - RhoA axis. Freiburg: Universität, 2013.

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12

Veillette, Christian J. H. Role of endothelin-1 in regulation of osteoblast differentiation and vascular endothelial growth factor-A in cell populations from fetal rat calvaria. Ottawa: National Library of Canada, 2002.

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13

Bland, Rosemary. Studies of thyroid hormone action in osteoblasts. Birmingham: University of Birmingham, 1996.

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14

Makinistoglu, Munevver. HDAC4 Integrate PTH and Sympathetic Signaling In Osteoblasts. [New York, N.Y.?]: [publisher not identified], 2014.

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15

Kung, Vanessa. Estrogen related receptor [alpha], ERR[alpha], regulation of target genes in osteoblasts. Ottawa: National Library of Canada, 2003.

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16

Compston, Juliet. Osteoporosis and bone biology: The state of the art. London: International Medical Press, 2000.

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17

Luo, Laura Chun. Receptors for extracellular ATP and other nucleotides in osteoblastic cells. [Toronto: Faculty of Dentistry, University of Toronto], 1995.

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18

Shelton, Richard Michael. The effect of substratum charge on the interfacial behaviour of osteoblasts in vitro. Birmingham: University of Birmingham, 1989.

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19

Mayeenuddin, Linnia H. Modulation of PTH-mediated signal transduction in osteoblasts by factors regulating cellular growth. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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20

National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging (1994 Washington, D.C.). National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging: Washington, DC, March 1-2, 1994. Edited by Robey Pamela Gehron 1952-, Sherman Sherry, National Institute of Dental Research (U.S.), and National Institute on Aging. New York, NY: Springer International, 1995.

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21

Walker, Lesley Margaret. The effect of mechanical and hormonal stimuli on femur derived osteoblasts; intracellular calcium fluxes and calcium channels. Birmingham: University of Birmingham, 1998.

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22

Crothers, Kristina A. Effects of Tamoxifen on Prostaglandin E2 induced insulin-like growth factor I expression in fetal rat osteoblasts. [New Haven, Conn: s.n.], 1997.

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23

David, Evered, Harnett Sara, and Ciba Foundation, eds. Cell and molecular biology of vertebrate hard tissues. Chichester, UK: Wiley, 1988.

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24

H, Helfrich Miep, and Ralston Stuart, eds. Bone research protocols. Totowa, N.J: Humana Press, 2003.

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25

H, Helfrich Miep, and Ralston Stuart, eds. Bone research protocols. Totowa, N.J: Humana Press, 2003.

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26

Tai, Victoria. The effects of leukotriene Bb4s on osteoclast formation and osteoclastic bone resorption and the role of osteoblastic cells in these processes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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27

service), ScienceDirect (Online, ed. Osteoimmunology: Interactions of the immune and skeletal systems. Amsterdam: Academic, 2011.

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28

R, Arnett Timothy, and Henderson Brian, eds. Methods in bone biology. London: Chapman & Hall, 1998.

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29

Zaidi, Mone. Osteoclast-Osteoblast. Jai Pr, 1999.

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30

Dixon, Samuel Jeffrey. Electrophysiology of a clonal osteoblast-like cell line. 1986.

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31

Raouf, Afshin. Role of Ets1 and Ets2 in osteoblast differentiation and bone formation. 2002.

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32

Rosenberg, Nahum. Autologous Bone Grafting and Regeneration: Clinical Applications of Biophysical Osteoblast Stimulation. Springer International Publishing AG, 2022.

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33

Anderson, Gail I. Osteoblast involvement in the formation and activation of osteoclasts in vitro. 1996.

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34

Skeletal collagen turnover by the osteoblast: Final technical report for NAG2-454. [Washington, DC: National Aeronautics and Space Administration, 1997.

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35

Cell Culture Methods for the Selection of Osteoblast-Like Cells from thePeriodontal Ligament. Storming Media, 1998.

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36

Turkson, Kursad *. Analysis of the osteoblast lineage: use of a cell culture model and monoclonal antibodies. 1991.

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37

Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.

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38

Vali, Bahareh. Effects of green tea epigallocatechin-3-gallate (EGCG) on the formation of mineralized bone nodules by human osteoblast-like cells. 2005.

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39

J. Singh, Parminder, and Rohit Kotnis. The musculoskeletal system: structure and function. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.0003.

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♦ Structure of bone is comprised of cells, matrix, and water♦ Bone consists broadly of three surfaces (periosteal, endosteal, and Haversian) and two membranes (periosteum and endosteum)♦ The blood supply of bone is derived from four main routes (nutrient, metaphyseal, epiphyseal, and periosteal arteries)♦ There are three main types of cells in bone (osteoblast, osteocyte, and osteoclast)♦ The matrix is a composite material consisting of an organic and an inorganic component♦ Two types of bone formation are intramembranous and endochondral ossification♦ The skeleton is also involved in the vital homeostasis of calcium and phosphate.

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40

Osteoblasts: Morphology, Functions and Clinical Implications. Nova Science Pub Inc, 2013.

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41

Frost, Anders. Effects of Inflammatory Mediators on Human Osteoblasts. Uppsala Universitet, 1999.

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42

Cheung, Ricky. Modulation of parathyroid hormone receptor signal transduction pathways in osteoblasts. 2005.

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43

(Editor), Juliet Compston, and Stuart Ralston (Editor), eds. Osteoporosis and Bone Biology - the State of the Art. International Medical Press, 2000.

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44

Basso, Nick. The effect of loading status on osteoprogenitors, osteoblasts, chondrocytes and bone formation in the rat. 2006.

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45

Ramminger, Andrés Fernández-Tenllado. Adhäsions- und Proliferationsverhalten von Osteoblasten und Keratinozyten auf verschiedenen Oberflächen von Titanimplantaten. 2008.

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46

Erclik, Mary S. Signaling mechanisms of parathyroid hormone regulation of insulin-like growth factor binding protein-5 in osteoblasts. 2006.

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47

Clarke, Noel W. Metastatic disease in prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.

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Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.

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48

Bone Research Protocols (Methods in Molecular Medicine). Humana Press, 2003.

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49

Helfrich, Miep H., and Stuart H. Ralston. Bone Research Protocols. Humana Press, 2016.

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50

Helfrich, Miep H., and Stuart H. Ralston. Bone Research Protocols. Humana Press, 2010.

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