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Thematische Bibliographien / Cartilage cells / Bücher

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Bücher zum Thema „Cartilage cells“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 5. März 2023

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1

1933-, Malinin Theodore I., Hrsg. Microscopic and histochemical manifestations of hyaline cartilage dynamics. Jena: Urban & Fischer Verlag, 1999.

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2

Malinin, George I. Microscopic and histochemical manifestations of hyaline cartilage dynamics. Jena, Germany: Urban & Fischer, 1999.

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3

F, Stoltz J., und International Symposium on Mechanobiology of Cartilage and Chondrocyte (1st : 1999 : Sainte-Maxime, France), Hrsg. Mechanobiology: Cartilage and chondrocyte. Amsterdam: IOS Press, 2000.

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4

Khan, Wasim S. Stem cells and cartilage tissue engineering approaches to orthopaedic surgery. Hauppauge, N.Y: Nova Science Publishers, 2009.

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5

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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6

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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7

International Workshop on Cells and Cytokines in Bone and Cartilage (4th 1992 Davos, Switzerland). Fourth Workshop on Cells and Cytokines in Bone and Cartilage: January 11-14, 1992, Davos, Switzerland : abstracts. New York, N.Y: Springer International, 1992.

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8

F, Stoltz J., Hrsg. Mechanobiology: Cartilage and chondrocyte. Amsterdam: IOS Press, 2006.

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9

Mechanobiology: Cartilage and chondrocyte. Amsterdam: IOS Press, 2008.

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10

Sampat, Sonal Ravin. Optimization of Culture Conditions for Cartilage Tissue Engineering Using Synovium-Derived Stem Cells. [New York, N.Y.?]: [publisher not identified], 2014.

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11

Tetlow, Lynne Christine. Histopathology of the rheumatoid lesion: Mast cells, metalloproteinases and cytokinesat sites of cartilage erosion. Manchester: University of Manchester, 1996.

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12

Regulation of Chondrogenesis in Human Mesenchymal Stem Cells by Cartilage Extracellular Matrix and Therapeutic Applications. [New York, N.Y.?]: [publisher not identified], 2018.

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13

Richard, Barrett-Jolley, Beck F. (Friedrich) 1927-, Bondy Carolyn A, Clascá F, Frotscher M. (Michael) 1947-, Haines Duane E, Hirokawa Nobutaka et al., Hrsg. Facilitative Glucose Transporters in Articular Chondrocytes: Expression, Distribution and Functional Regulation of GLUT Isoforms by Hypoxia, Hypoxia Mimetics, Growth Factors and Pro-Inflammatory Cytokines. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2008.

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14

M, Shapiro Irving, Boyan Barbara und Anderson H. Clarke, Hrsg. The growth plate. Amsterdam: IOS Press, 2002.

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15

Monique, Adolphe, Hrsg. Biological regulation of the chondrocytes. Boca Raton, Fla: CRC Press, 1992.

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16

Embryonic stem cell therapy for osteo-degenerative diseases: Methods and protocols. New York, NY: Humana Press, 2011.

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17

Gregory, Bock, und Goode Jamie, Hrsg. Tissue engineering of cartilage and bone. Chichester, West Sussex: J. Wiley, 2003.

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18

Jūryūshi Ikagaku Sentā. Shinpojūmu "Saisei Iryō to Bunshi Imējingu". Dai 3-kai Jūryūshi Ikagaku Sentā Shinpojūmu Saisei Iryō to Bunshi Imējingu. Chiba-ken Chiba-shi: Hōshasen Igaku Sōgō Kenkyūjo, 2004.

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19

Lau, Wing Fun. Regulation of cartilage differentiation and formation in a chondrogenic cell line by retinoic acid, dexamethasone and 1,25-dihydroxyvitamin Df3d. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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20

Cardew, Gail. The molecular basis of skeletogenesis. Chichester: Wiley, 2001.

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21

Taehakkyo, Chŏnbuk, Hrsg. Nano haibŭridŭ sojae wa kanyŏp chulgi sepʻo rŭl iyonghan kol mit yŏnʼgol chaesaeng kisul kaebal e kwanhan yŏnʼgu: Chʻoejong yŏnʼgu kaebal kyŏlgwa pogosŏ = A study on the development of cartilage and bone regeneration by nanohybrid biomaterials with mesenchymal stem cell. [Seoul]: Pogŏn Pokchibu, 2004.

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22

Sabatini, Massimo, Philippe Pastoureau und Frédéric de Ceuninck. Cartilage and Osteoarthritis. Humana Press, 2010.

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23

Sabatini, Massimo, Philippe Pastoureau und Frédéric de Ceuninck. Cartilage and Osteoarthritis. Humana Press, 2010.

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24

Cartilage and osteoarthritis. Totowa, NJ: Humana Press, 2004.

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25

(Editor), Massimo Sabatini, Philippe Pastoureau (Editor) und FrTdTric De Ceuninck (Editor), Hrsg. Cartilage and Osteoarthritis (Methods in Molecular Medicine). Humana Press, 2004.

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26

(Foreword), L. Peterson, B. J. Cole (Foreword) und Riley J. Williams (Editor), Hrsg. Cartilage Repair Strategies. Humana Press, 2007.

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27

(Editor), Frédéric De Ceuninck, Massimo Sabatini (Editor) und Philippe Pastoureau (Editor), Hrsg. Cartilage and Osteoarthritis (Methods in Molecular Medicine). Humana Press, 2004.

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28

Mechanobiology: Cartilage and Chondrocyte (Biomedical and Health Research). Ios Pr Inc, 2002.

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29

Stoltz, J. F. Mechanobiology: Cartilage And Chondrocyte (Biomedical and Health Research). Ios Pr Inc, 2004.

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30

Muldrew, Kenneth B. The osmotic rupture hypothesis and its application to the cryopreservation of articular cartilage. 1993.

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31

MECHANOBIOLOG, INTERNATIONAL SYMPOSIUM ON, und J. F. Stoltz. Mechanobiology: Cartilage and Chondrocyte, Vol. 4 (Biomedical and Health Research, Vol. 68) (Biomedical and Health Research). IOS Press, 2006.

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32

The Effect of Titanium Surface Roughness on Growth, Differentiation, and Protein Synthesis of Cartilage and Bone Cells. Storming Media, 1996.

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33

(Editor), Irving M. Shapiro, Barbara Boyan (Editor) und H. Clarke Anderson (Editor), Hrsg. The Growth Plate (Biomedical and Health Research, 54). Ios Pr Inc, 2002.

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34

Adolphe, Monique. Biological Regulation of the Chondrocytes. CRC Press LLC, 2022.

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35

Adolphe, Monique. Biological Regulation of the Chondrocytes. CRC Press LLC, 2022.

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36

Adolphe, Monique. Biological Regulation of the Chondrocytes. CRC Press LLC, 2022.

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37

Adolphe, Monique. Biological Regulation of the Chondrocytes. CRC Press LLC, 2022.

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38

Goldring, Steven R. Pathophysiology of periarticular bone changes in osteoarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0005.

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Under physiological conditions, the subchondral bone of diarthrodial joints such as the hip, knee, and phalanges forms an integrated biocomposite with the overlying calcified and hyaline articular cartilage that is optimally organized to transfer mechanical load. During the evolution of the osteoarthritic process both the periarticular bone and cartilage undergo marked changes in their structural and functional properties in response to adverse biomechanical and biological signals. These changes are mediated by bone cells that modify the architecture and properties of the bone through active cellular processes of modelling and remodelling. These same biomechanical and biological factors also affect chondrocytes in the cartilage matrix altering the composition and structure of the cartilage and further disrupting the homeostatic relationship between the cartilage and bone. This chapter reviews the structural alterations and cellular mechanisms involved in the pathogenesis of osteoarthritis bone pathology and discusses potential approaches for targeting bone remodelling to attenuate the progression of the osteoarthritic process.

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39

Pitzalis, Costantino, Frances Humby und Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.

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40

Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.

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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.

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41

Shakibaei, Mehdi, Constanze Csaki und Ali Mobasheri. Diverse Roles of Integrin Receptors in Articular Cartilage. Springer, 2008.

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42

Fernandes, Tiago Lazzaretti, Daniela Franco Bueno, Kazunori Shimomura, Zhenxing Shao und Andreas H. Gomoll, Hrsg. Tissue Engineering and Cell Therapy for Cartilage Restoration. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-145-0.

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43

Narcisi, Roberto, und Elena Jones, Hrsg. Cell-Based Approaches for Modulating Cartilage and Bone Phenotype. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-855-9.

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44

Thomas, Ranjeny, und Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.

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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.

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45

Diverse Roles Of Integrin Receptors In Articular Cartilage. Springer, 2008.

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46

Narcisi, Roberto, und Eric Farrell, Hrsg. Understanding and Modulating Bone and Cartilage Cell Fate for Regenerative Medicine. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-790-8.

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47

Tissue Engineering of Cartilage and Bone - No. 249 (Novartis Foundation Symposia). Wiley, 2003.

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48

Abhishek, Abhishek, und Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.

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49

Control of Tissue Damage (Research Monographs in Cell & Tissue Physiology). Elsevier Science Ltd, 2000.

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50

The Molecular Basis of Skeletogenesis No. 232. Wiley, 2001.

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