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Herniated Lumbar Intervertebral Discs Spontaneously Produce Matrix Metalloproteinases, Nitric Oxide, Interleukin-6, and Prostaglandin E2
- J. D. Kang, H. Georgescu, L. McIntyre-Larkin, M. Stefanovic-Racic, W. Donaldson, C. Evans
- 1 February 1996
Herniated lumbar discs were making spontaneously increased amounts of matrix metalloproteinases, nitric oxide, prostaglandin E2, and interleukin-6, which may be involved intimately in the biochemistry of disc degeneration and the pathophysiology of radiculopathy. Expand
Toward a Biochemical Understanding of Human Intervertebral Disc Degeneration and Herniation: Contributions of Nitric Oxide, Interleukins, Prostaglandin E2, and Matrix Metalloproteinases
Endogenously produced nitric oxide appears to have a strong inhibitory effect on the production of interleukin‐6, which suggests that autocrine mechanisms play an important role in the regulation of disc cell metabolism. Expand
Evaluation of adult equine bone marrow‐ and adipose‐derived progenitor cell chondrogenesis in hydrogel cultures
- J. Kisiday, P. Kopesky, C. Evans, A. Grodzinsky, C. McIlwraith, D. Frisbie
- Chemistry, Medicine
- Journal of orthopaedic research : official…
- 1 March 2008
Both protein and gene expression evidence of superior chondrogenesis of BM‐MSCs relative to ADPCs are shown. Expand
Biologics for tendon repair☆
This review describes and critically assess the current strategies for enhancing tendon repair by biological means, mainly of applying growth factors, stem cells, natural biomaterials and genes, alone or in combination, to the site of tendon damage. Expand
Modulation of the biologic activity of the rabbit intervertebral disc by gene therapy: an in vivo study of adenovirus-mediated transfer of the human transforming growth factor beta 1 encoding gene.
The results of this study suggest that the intervertebral disc is an appropriate site for adenovirus-mediated transfer of exogenous genes and subsequent production of therapeutic growth factors. Expand
The Natural History of the Anterior Cruciate Ligament-Deficient Knee
- M. Cameron, A. Buchgraber, +4 authors C. Evans
- The American journal of sports medicine
- 1 November 1997
A persistent and evolving disturbance in cytokine and keratan sulfate profiles within the anterior cruciate ligament-deficient knee is revealed, suggesting an important biochemical dimension to the development of osteoarthritis there. Expand
Synovial fibroblasts spread rheumatoid arthritis to unaffected joints
The hypothesis that the characteristic clinical phenomenon of destructive arthritis spreading between joints is mediated, at least in part, by the transmigration of activated RASFs is supported. Expand
Direct adenovirus-mediated gene transfer of interleukin 1 and tumor necrosis factor alpha soluble receptors to rabbit knees with experimental arthritis has local and distal anti-arthritic effects.
- S. Ghivizzani, E. Lechman, +4 authors P. Robbins
- Biology, Medicine
- Proceedings of the National Academy of Sciences…
- 14 April 1998
Results suggest that local intra-articular gene transfer could be used to treat systemic polyarticular arthritides and suggest that sustained local inhibition of disease activity in one joint may confer an anti-arthritic effect on other joints. Expand
Articular chondrocytes synthesize nitric oxide in response to cytokines and lipopolysaccharide.
- J. Stadler, M. Stefanovic-Racic, +5 authors C. Evans
- Chemistry, Medicine
- Journal of immunology
- 1 December 1991
IL-1 induces the biosynthesis of nitric oxide (.N = O) by articular chondrocytes and enhances the synthesis of both gelatinase and PGE2 after activation with a combination of IL-1, LPS, and TNF-alpha. Expand
Genetic enhancement of matrix synthesis by articular chondrocytes: comparison of different growth factor genes in the presence and absence of interleukin-1.
Transfer of growth factor genes to articular chondrocytes can greatly increase matrix synthesis in vitro, even in the presence of the inflammatory cytokine IL-1, encouraging the further development of gene therapy for the repair of damaged cartilage. Expand