In each of
these cases you can go to the Medline site
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
and enter
the PMID number to bring up the abstract.
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Life Sci. 2002 May 31;71(2):139-51.
PMID: 12031684 [PubMed - indexed for MEDLINE]
GH administration and renal IGF-I system in arthritic rats.
Ibanez de Caceres I, Priego T, Martin AI, Lopez-Calderon A, Villanua MA.
CONCLUSION: These data suggest that experimental arthritis causes renal dysfunction and GH treatment can ameliorate this effect.
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J Bone Joint Surg Br 2002 Mar;84(2):276-88 Related Articles, Links
PMID: 11922373 [PubMed - indexed for MEDLINE]
Insulin-like growth factor-I enhances cell-based repair of articular cartilage.
Fortier LA, Mohammed HO, Lust G, Nixon AJ.
Cornell University College of Veterinary Medicine, Ithaca, New York 14853, USA.
Gross filling of defects was improved, and the tissue contained a higher proportion of cells producing type-II collagen. Measurements of collagen type II showed improved levels in IGF-I-treated defects, supporting in situ hybridisation and immunohistochemical assessments of the defects. IGF-I improves the repair capabilities of chondrocyte-fibrin grafts in large full-thickness repair models.
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Gene Ther 2001 Oct;8(19):1443-9 Related Articles, Links
PMID: 11593356 [PubMed - indexed for MEDLINE]
Overexpression of human insulin-like growth factor-I promotes new tissue formation in an ex vivo model of articular chondrocyte transplantation.
Madry H, Zurakowski D, Trippel SB.
Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Articular cartilage, the tissue that forms the gliding surface of joints, has a poor regenerative capacity. Insulin-like growth factor-I (IGF-I) is a polypeptide that is anabolic and mitogenic for cartilage.
These results identify a mechanism by which IGF-I may simultaneously promote chondrogenesis and shift cartilage homeostasis in an anabolic direction. The data further suggest that therapeutic growth factor gene transfer may be applicable to articular cartilage.
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J Orthop Res 2001 Jul;19(4):720-8 Related Articles, Links
PMID: 11518284 [PubMed - indexed for MEDLINE]
Insulin-like growth factor-I gene expression patterns during spontaneous repair of acute articular cartilage injury.
Fortier LA, Balkman CE, Sandell LJ, Ratcliffe A, Nixon AJ.
Comparative Orthopaedics Laboratory, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
This study evaluated the constitutive insulin-like growth factor-I (IGF-I) gene expression pattern in spontaneously healing cartilage defects over the course of 16 weeks, and correlated the tissue morphology and matrix gene expression with IGF-I mRNA levels.
In conclusion, this study demonstrated that the spontaneous healing of articular defects was accompanied by a temporal fluctuation in IGF-I gene expression which was discoordinate to the steady rise in expression of cartilage matrix molecules such as procollagen type II.
Association between insulin-like growth factor status and physical activity levels in rheumatoid arthritis.
Lemmey A, Maddison P, Breslin A, Cassar P, Hasso N, McCann R, Whellams E, Holly J.
CONCLUSION: Our results indicate that the reduction in circulating IGF proteins observed in our patients is more related to their sedentary lifestyle than to the inflammatory process. This conclusion is in agreement with reports that show that highly active individuals typically exhibit higher levels of systemic IGF proteins than age matched sedentary controls.
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J Orthop Res 2001 Jan;19(1):11-7
PMID: 11332605 [PubMed - indexed for MEDLINE]
The effect of dynamic compression on the response of articular cartilage to insulin-like growth factor-I.
Bonassar LJ, Grodzinsky AJ, Frank EH, Davila SG, Bhaktav NR, Trippel SB.
Orthopaedic Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.
Articular cartilage is routinely subjected to mechanical forces and to cell-regulatory molecules. Previous studies have shown that mechanical stimuli can influence articular chondrocyte metabolic activity, and biochemical studies have shown that growth factors and cytokines control many of the same cell functions. Little is known, however, of the relationships or interplay, if any, between these two key components of the articular environment. This study investigated the comparative and interactive effects of low amplitude, sinusoidal, dynamic compression and insulin-like growth factor-I (IGF-I), a polypeptide in synovial fluid that is anabolic for cartilage.
Thus, dynamic compression accelerated the biosynthetic response to IGF-I and increased transport of IGF-I into the articular cartilage matrix, suggesting that, in addition to independently stimulating articular chondrocytes, cyclic compression may improve the access of soluble growth factors to these relatively isolated cells.
Duncan Crow