Download Cartilage: Volume 1: Physiology and Development by Susanne Grässel, Attila Aszódi PDF

By Susanne Grässel, Attila Aszódi

In 3 Volumes this mini e-book sequence provides present wisdom and new views on cartilage as a really good but flexible tissue. this primary quantity presents a entire evaluate at the uncomplicated composition and improvement of cartilaginous tissues via the outline of the main signaling pathways which keep an eye on cartilage morphogenesis and function.
This ebook addresses Professors, researchers and PhD scholars who're drawn to musculoskeletal and cartilage biology.

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Extra info for Cartilage: Volume 1: Physiology and Development

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The long bones are shortened, contain a thickened cortical collar, and lack endochondral bone and epiphyseal growth plate; the vertebral arches are rudimentary and do not fuse. In addition, Col2a1-null mice are unable to dismantle the notochord. This defect is associated with the inability to develop intervertebral disks (IVDs) (Aszodi et al. 1998a). Previous studies showed that in both Col2a1-null mice and in a patient with achondrogenesis type II carrying a COL2A1 mutation collagen II is completely absent in the cartilage, whereas collagen I was found to be ectopically expressed in the cartilage (Aszodi et al.

In adult articular cartilage, for example, thin fibrils near the joint cavity preferentially run parallel to the surface, since lateral forces predominate in this region. In the interterritorial regions of the deep zones, in contrast, wider fibrils are arranged perpendicularly to the surface to strengthen the tissue in the direction along the axis of the bones. A prominent feature of the fibrils in developing and in immature cartilage is their strictly uniform diameter of about 20 nm and their more random orientation.

2014). Recently, genome wide association studies (GWAS) identified a single nucleotide polymorphism (SNP) rs2615977 to be associated with osteoarthritis (OA) and located in intron 31 of COL11A1, comprising a strong candidate gene for this degenerative musculoskeletal disease. However, a study by Raine et al. did not provide evidence for a correlation between the OA-associated SNP rs2615977 and COL11A1 allelic expression imbalance (Raine et al. 2013). The lack of a correlation 36 S. Grässel between the OA-associated SNP rs2615977 and COL11A1 expression implies that the association marked by this SNP is operating by a route other than an effect on the expression of the gene in mature cartilage.

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