Co-localization of insulin-like growth factor binding protein 3 and fibronectin in human articular cartilage.

Objective: The anabolic cytokine insulin-like growth factor I (IGF-I) stimulates chondrocyte synthesis of matrix macromolecules and several lines of evidence suggest that it has a major role in maintaining articular cartilage and possibly in cartilage repair. Despite the apparent importance of IGF-I in articular cartilage metabolism and its potential importance in joint diseases, little is known about the regulation of IGF-I activity within the tissue. Insulin-like growth factor binding proteins (IGFBPs) bind IGF-I and can modify its activity.

Reversible suppression of in vitro biomineralization by activation of protein kinase A.

Parathyroid hormone (PTH-(1-34)) potently suppresses apatite deposition in osteoblastic cultures. These inhibitory effects are mediated through signaling events following PTH receptor binding. Using both selective inhibitors and activators of protein kinase A (PKA), this study shows that a transient activation of PKA is sufficient to account for PTH's inhibition of apatite deposition.

Damage control mechanisms in articular cartilage: the role of the insulin-like growth factor I axis.

Articular chondrocytes maintain cartilage throughout life by replacing lost or damaged matrix with freshly synthesized material. Synthesis activity is regulated, rapidly increasing to well above basal levels in response to cartilage injury. Such responses suggest that synthesis activity is linked to the rate of matrix loss by endogenous "damage control" mechanisms.

Rapidly forming apatitic mineral in an osteoblastic cell line (UMR 106-01 BSP).

This study evaluated a rapid biomineralization phenomenon exhibited by an osteoblastic cell line, UMR 106-01 BSP, when treated with either organic phosphates [beta-glycerophosphate (beta-GP), Ser-P, or Thr-P], inorganic phosphate (P(i)), or calcium. In a dose-dependent manner, these agents (2-10 mM) stimulated confluent cultures to deposit mineral in the cell layer (ED50 of approximately 4.6 mM for beta-GP (30 +/- 2 nmol Ca2+/microgram DNA) and approximately 3.

Comparative effects of gentamicin and tobramycin on excretion of N-acetyl-beta-D-glucosaminidase.

Patients receiving gentamicin or tobramycin were studied to determine whether there were differences in the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) between the two groups. The average daily increases in NAG excretion were significantly higher in the group receiving gentamicin. In individual patients, the best correlation with nephrotoxicity was with high initial rates of NAG excretion.