Bibliografie tematiche / Bone resorption – Molecular aspects

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Letteratura scientifica selezionata sul tema "Bone resorption – Molecular aspects"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 1 febbraio 2022

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Articoli di riviste sul tema "Bone resorption – Molecular aspects"

1

Gao, Yongguang, Suryaji Patil, and Jingxian Jia. "The Development of Molecular Biology of Osteoporosis." International Journal of Molecular Sciences 22, no. 15 (July 30, 2021): 8182. http://dx.doi.org/10.3390/ijms22158182.

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Abstract (sommario):
Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these m
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2

Asmah, Nur. "Molecular aspects of Enterococcus faecalis virulence." Journal of Syiah Kuala Dentistry Society 5, no. 2 (February 15, 2021): 89–94. http://dx.doi.org/10.24815/jds.v5i2.20020.

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The Enterococcus faecalis (E. Faecalis) virulence factor plays an essential role in the persistence of root canal infection. Virulence factors of Enterococcus faecalis such as lipoteichoic acid, extracellular superoxide, gelatinase, hyaluronidase, and cytolysin are known to increase the ability of Enterococcus faecalis to induce inflammatory processes, colonization formation, and increase resistance. The virulence factor of E. faecalis is mediated by LTA, which has pattern recognition receptors for cytokine release, bone resorption and triggers apoptosis of osteoblasts, osteoclasts, periodonta
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Marini, Francesca, Francesca Giusti, Teresa Iantomasi, and Maria Luisa Brandi. "Congenital Metabolic Bone Disorders as a Cause of Bone Fragility." International Journal of Molecular Sciences 22, no. 19 (September 24, 2021): 10281. http://dx.doi.org/10.3390/ijms221910281.

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Abstract (sommario):
Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of high-impact trauma. The most common cause of bone fragility is primary osteoporosis in the elderly. However, bone fragility can manifest at any age, within the context of a wide spectrum of congenital rare bone metabolic diseases in which the inherited genetic defect alters correct bone modeling and remodeling at different point
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Driessler, Frank, and Paul A. Baldock. "Hypothalamic regulation of bone." Journal of Molecular Endocrinology 45, no. 4 (July 26, 2010): 175–81. http://dx.doi.org/10.1677/jme-10-0015.

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Abstract (sommario):
On initial inspection, bone remodeling, the process whereby the skeleton adapts through time, appears to be relatively simple. Two cell types, the bone-forming osteoblasts and the bone-resorbing osteoclasts, interact to keep bone mass relatively stable throughout adult life. However, the complexity of the regulatory influences on these cells is continuing to expand our understanding of the intricacy of skeletal physiology and also the interactions between other organ systems and bone. One such example of the broadening of understanding in this field has occurred in the last decade with study o
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Leightner, Amanda C., Carina Mello Guimaraes Meyers, Michael D. Evans, Kim C. Mansky, Rajaram Gopalakrishnan, and Eric D. Jensen. "Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases." International Journal of Molecular Sciences 21, no. 3 (February 5, 2020): 1056. http://dx.doi.org/10.3390/ijms21031056.

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Abstract (sommario):
Balanced osteoclast and osteoblast activity is necessary for skeletal health, whereas unbalanced osteoclast activity causes bone loss in many skeletal conditions. A better understanding of pathways that regulate osteoclast differentiation and activity is necessary for the development of new therapies to better manage bone resorption. The roles of Protein Kinase D (PKD) family of serine/threonine kinases in osteoclasts have not been well characterized. In this study we use immunofluorescence analysis to reveal that PKD2 and PKD3, the isoforms expressed in osteoclasts, are found in the nucleus a
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Berardi, S., A. Corrado, N. Maruotti, D. Cici, and F. P. Cantatore. "Osteoblast role in the pathogenesis of rheumatoid arthritis." Molecular Biology Reports 48, no. 3 (March 2021): 2843–52. http://dx.doi.org/10.1007/s11033-021-06288-y.

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AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid ar
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7

Kajarabille, Naroa, Javier Díaz-Castro, Silvia Hijano, Magdalena López-Frías, Inmaculada López-Aliaga, and Julio J. Ochoa. "A New Insight to Bone Turnover: Role of -3 Polyunsaturated Fatty Acids." Scientific World Journal 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/589641.

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Abstract (sommario):
Background. Evidence has shown that long-chain polyunsaturated fatty acids (LCPUFA), especially theω-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are beneficial for bone health and turnover.Objectives. This review summarizes findings from bothin vivoandin vitrostudies and the effects of LC PUFA on bone metabolism, as well as the relationship with the oxidative stress, the inflammatory process, and obesity.Results. Some studies in humans indicate that LCPUFA can increase bone formation, affect peak bone mass in adolescents, and reduce bone loss. However, the
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Lin, Peiya, Hiromi Niimi, Yujin Ohsugi, Yosuke Tsuchiya, Tsuyoshi Shimohira, Keiji Komatsu, Anhao Liu, et al. "Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8900. http://dx.doi.org/10.3390/ijms22168900.

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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue d
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Kaur, Malkiet, Manju Nagpal, and Manjinder Singh. "Osteoblast-n-Osteoclast: Making Headway to Osteoporosis Treatment." Current Drug Targets 21, no. 16 (December 14, 2020): 1640–51. http://dx.doi.org/10.2174/1389450121666200731173522.

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Abstract (sommario):
Background: Bone is a dynamic tissue that continuously undergoes the modeling and remodeling process to maintain its strength and firmness. Bone remodeling is determined by the functioning of osteoblast and osteoclast cells. The imbalance between the functioning of osteoclast and osteoblast cells leads to osteoporosis. Osteoporosis is divided into primary and secondary osteoporosis. Generally, osteoporosis is diagnosed by measuring bone mineral density (BMD) and various osteoblast and osteoclast cell markers. Methods: Relevant literature reports have been studied and data has been collected us
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Gatti, Martina, Francesca Beretti, Manuela Zavatti, Emma Bertucci, Soraia Ribeiro Luz, Carla Palumbo, and Tullia Maraldi. "Amniotic Fluid Stem Cell-Derived Extracellular Vesicles Counteract Steroid-Induced Osteoporosis In Vitro." International Journal of Molecular Sciences 22, no. 1 (December 22, 2020): 38. http://dx.doi.org/10.3390/ijms22010038.

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Background—Osteoporosis is characterized by defects in both quality and quantity of bone tissue, which imply high susceptibility to fractures with limitations of autonomy. Current therapies for osteoporosis are mostly concentrated on how to inhibit bone resorption but give serious adverse effects. Therefore, more effective and safer therapies are needed that even encourage bone formation. Here we examined the effect of extracellular vesicles secreted by human amniotic fluid stem cells (AFSC) (AFSC-EV) on a model of osteoporosis in vitro. Methods—human AFSC-EV were added to the culture medium o
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Tesi sul tema "Bone resorption – Molecular aspects"

1

Cheng, Tak Sum. "Molecular identification and characterization of novel osteoclast V-ATPase subunits." University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0068.

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[Truncated abstract] Osteoclasts are multinucleated giant cells responsible for the resorption of the mineralized bone matrix during the process of bone remodelling. During activation towards bone resorption, polarization of the osteoclast results in the formation of a unique plasma membrane, the ruffled border, the actual resorptive organelle of the osteoclast. Through this domain protons are actively pumped into the resorption lacuna creating an acidic microenvironment that favours the dissolution of the mineralized bone matrix. The polarised secretion of protons is carried out by the action
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Wang, Cathy Ting-Peng. "Molecular dissection of RANKL signaling pathways in osteoclasts." University of Western Australia. School of Surgery and Pathology, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0037.

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[Truncated abstract] Bone remodeling is intricately regulated by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The elevation in osteoclast number and/or activity is a major hallmark of several common pathological bone disorders including post-menopausal osteoporosis, osteoarthritis, Paget's disease, and tumour-mediated osteolysis. Receptor activator of nuclear factor kappa B ligand (RANKL) is a key cytokine for osteoclast differentiation and activation. The association of RANKL to its cognate receptor, RANK, which is expressed on osteoclast precursors and mature o
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Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.

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Tan, Jamie We-Yin. "The investigation of RANKL TNF-like core domain by truncation mutation." University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0032.

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Abstract (sommario):
Osteoclasts are multinucleated cells found exclusively in bone and are derived from the haematopoietic cells of monocytes/macrophage lineage. The cell-to-cell interaction between osteoblastic/stromal cells and osteoclast precursor cells is necessary for osteoclastogenesis. Receptor Activator of NF-κB ligand (RANKL) was identified as a membrane-bound TNF ligand family member that is the ‘master’ cytokine expressed on osteoblastic/stromal cells, which stimulate osteoclastogenesis through cell-to-cell contact with osteoclast precursors. RANKL is considered to be a factor that is necessary and suf
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Hou, Peng. "Matrix metalloproteinases in the osteoclast, with special emphasis on the molecular cloning and the functional role of matrix metalloproteinase-12." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287350.

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Peng, Songlin, and 彭松林. "Investigation of the cellular and molecular mechanisms for the dual effect of strontium on bone." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45585167.

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Tkachenko, Evgeniy. "Measures of Individual Resorption Cavities in Three-Dimensional Images in Cancellous Bone." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301413780.

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Burger, Nicolaas Daniel Lombard. "Failure analysis of ultra-high molecular weight polyethyelene acetabular cups." Pretoria : [s.n.], 2005. http://upetd.up.ac.za/thesis/available/etd-12142006-134036.

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Mbimba, Thomas S. Jr. "TRAFICKING PROTEIN PARTICLE COMPLEX (TRAPPC) -9:A NOVEL PROTEIN REGULATOR OF NF-kB MEDIATED BONE FORMATION AND RESORPTION." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1448841594.

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Cheng, Yin-wo, and 鄭燕和. "Molecular basis for the increased osteoblast activity in a mouse modelwith hyperostosis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B34612981.

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Libri sul tema "Bone resorption – Molecular aspects"

1

Wackym, Phillip A. Molecular temporal bone pathology, parts III and IV. Philadelphia, PA: Lippincott-Raven, 1998.

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2

Raisz, Lawrence G. (Lawrence Gideon), 1925-, Martin T. John, and ScienceDirect (Online service), eds. Principles of bone biology. 3rd ed. Amsterdam: Elsevier, 2008.

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Rosen, Vicki. The cellular and molecular basis of bone formation and repair. New York: Springer, 1995.

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1957-, Thies Robert Scott, ed. The cellular and molecular basis of bone formation and repair. Austin: R.G. Landes, 1995.

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Dietz, Georg. Calcium hydroxide and bone regeneration: Odontological aspects of induced osteogenesis in experiment and clinical practice. München: G. Dietz, 1998.

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

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(Foreword), G. A. Rodan, Felix Bronner (Editor), and Mary C. Farach-Carson (Editor), eds. Bone Formation (Topics in Bone Biology). Springer, 2003.

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Gurmit, Singh, and Orr F. William, eds. Bone metastasis and molecular mechanisms: Pathophysiology. Dordrecht: Kluwer Academic, 2004.

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Orr, William, and Gurmit Singh. Bone Metastasis and Molecular Mechanisms: Pathophysiology. Springer-Verlag New York Inc., 2004.

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Singh, Gurmit. Bone Metastasis and Molecular Mechanisms: Pathophysiology. Springer, 2010.

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Capitoli di libri sul tema "Bone resorption – Molecular aspects"

1

Woo, Je-Tae, Yasuo Ohba, Kahori Tagami, Koji Sumitani, Kohji Yamaguchi, Tomoko Tsuji, Takao Kataoka, and Kazuo Nagai. "Low Molecular Weight Microbial Metabolites that Suppress Bone Resorption by Inhibiting Vacuolar Type Proton Pump Activity of Osteoclasts." In Animal Cell Technology: Basic & Applied Aspects, 627–32. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5746-9_102.

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Russell, Graham, Gabrielle Mueller, Claire Shipman, and Peter Croucher. "Clinical Disorders of Bone Resorption." In The Molecular Basis of Skeletogenesis, 251–71. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470846658.ch17.

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Kiyoi, Takeshi. "Bone Resorption Activity in Mature Osteoclasts." In Methods in Molecular Biology, 215–22. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8802-0_22.

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Bab, Itai A., and Jona J. Sela. "Cellular and Molecular Aspects of Bone Repair." In Principles of Bone Regeneration, 11–41. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2059-0_2.

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Biosse-Duplan, Martin, William C. Horne, and Roland Baron. "Cell and Molecular Biology of the Osteoclast and Bone Resorption." In Mineralized Tissues in Oral and Craniofacial Science, 17–27. West Sussex, UK: John Wiley & Sons, Inc.,, 2013. http://dx.doi.org/10.1002/9781118704868.ch3.

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Winston, Drew J. "Cytomegalovirus Infection in Bone Marrow Transplantation." In Molecular Aspects of Human Cytomegalovirus Diseases, 183–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_11.

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Brunetti, Giacomina, Angela Oranger, Silvia Colucci, and Maria Grano. "Experimental Model for Studying the Involvement of Regulatory Cytotoxic T Cells in Bone Resorption." In Methods in Molecular Biology, 269–81. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1158-5_15.

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Tsuji, Tomoko, Kohji Yamaguchi, Mika Yada, Kaoru Yamada, and Daisuke Uemura. "Norzoanthamine Suppresses PTH-Stimulated IL-6 Production in Vitro and Bone Resorption in Vivo." In Animal Cell Technology: Basic & Applied Aspects, 137–41. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5161-0_24.

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Dawidowska, Małgorzata. "Isolation of Mononuclear Cells from Human Blood and Bone Marrow by Density Gradient Centrifugation." In Molecular Aspects of Hematologic Malignancies, 305–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29467-9_19.

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Wiren, Kristine M. "Androgen Action in Bone: Basic Cellular and Molecular Aspects." In Osteoporosis, 359–83. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-459-9_16.

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Atti di convegni sul tema "Bone resorption – Molecular aspects"

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Ungur, Petru, Elisabeta Patcas, Petru A. Pop, Silviu Corbu, and Florin M. Marcu. "Theoretical and Practical Aspects About Bio-Lubrication of Synovial Joints by Radioactive Molecular Treatment." In ASME 2008 9th Biennial Conference on Engineering Systems Design and Analysis. ASMEDC, 2008. http://dx.doi.org/10.1115/esda2008-59160.

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The paper has presented the result of tests and researches realized at our university and Oncology Clinical Hospital from Oradea, Radiotherapy Section, about improving of biolubrication between cartilages in relative moving of synovial joints with osteoarthritis, having slow evolution under non-conventional treatment of irradiation with gamma ray. By radioactive molecular treatment of synovial joints with gamma ray, type hinge of knee and spheres of disorder hip (gon-arthrosis and cox-arthrosis), changed molecular structures of porous cartilages and of synovial fluid in contact. All these due
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Hauert, R. "A Review of DLC Coatings for Biological Applications." In World Tribology Congress III. ASMEDC, 2005. http://dx.doi.org/10.1115/wtc2005-63879.

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Diamond-like carbon (DLC) is a class of materials with outstanding mechanical, tribological and biological properties. From in-vitro experiments, it is known that by incorporating other elements into the DLC film, the ratios of the different proteins adsorbed on the surface can be changed. These proteins will then subsequently control cell attachment, cell proliferation and cell differentiation. In a total hip joint replacement, the metallic femoral head, which slides against a polyethylene pan, causes polymeric wear debris. These wear particles may then trigger inflammatory reactions, resulti
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