Integrin-associated protein is a receptor for the C-terminal domain of thrombospondin.

The C-terminal "cell-binding domain" (CBD) of thrombospondin-1 (TS1) is a binding site for many cell types. Cell-binding peptides based on the sequence RFYVVM from the CBD of TS1 affinity label a 52-kDa cell surface glycoprotein, which we show is integrin-associated protein (IAP or CD47). IAP associates with alpha v beta 3 and thereby modulates the activity of several integrins. Cells that express IAP bind strongly to TS1, the CBD, and its active cell-binding peptides while IAP negative cells do not. The 52-kDa protein is affinity labeled on IAP-positive but not IAP-negative cells, and monoclonal antibodies against IAP specifically immunoprecipitate the affinity-labeled 52-kDa protein from lysates of IAP-positive cells. Consistent with the association of IAP with alpha v beta 3 integrin, the labeled 52-kDa protein is immunoprecipitated by an anti-alpha v beta 3 antibody. Endothelial cells exhibit chemotaxis toward TS1 (at concentrations above 10 nM) and RFYVVM peptides. Chemotaxis to both agents is specifically inhibited by a function blocking anti-IAP monoclonal antibody. These data establish IAP (CD47) as a receptor for the CBD of TS1 and suggest a mechanism for the well established effects of the CBD on cell motility.

Detection of chrysotile asbestos in workers' urine.

Urinary asbestos concentrations were evaluated as an indicator of occupational exposure to chrysotile asbestos via inhalation and ingestion. Detection of asbestos in the urine represents the first step in developing a biological indicator of exposure. Such an indicator could be used to supplement exposure data from workplace air sampling. A biological indicator would be particularly valuable in evaluating workers with intermittent airborne asbestos exposures and in determining if airborne exposure results in penetration of asbestos through the lung or gastro-intestinal tract. Transmission electron microscopy was selected as the most sensitive technique for identification of all sizes of asbestos fibers which might appear in the urine. First morning void urine samples were obtained from six workers (occupationally exposed to chrysotile asbestos in a factory producing roof coatings) and from a control group (six individuals with no occupational exposure). The levels of chrysotile asbestos detected in the urine of five workers were significantly greater than the asbestos concentrations in matched field blanks (both on a number and mass basis). Field blanks were designed to detect asbestos in the urine samples due to contamination which might occur during urine collection. Also, the workers' urinary asbestos levels were significantly greater than the concentrations found in the control group (both on a number and mass basis). Finally, the levels of chrysotile asbestos detected in the urine of two of six controls were significantly greater than those in matched field blanks (both on a number and mass basis). Although the project was not specifically designed to correlate urinary and airborne asbestos concentrations, preliminary data indicated that a correlation did not exist between these factors.

Detection of chrysotile asbestos in workers' urine.

Urinary asbestos concentrations were evaluated as an indicator of occupational exposure to chrysotile asbestos via inhalation and ingestion. Detection of asbestos in the urine represents the first step in developing a biological indicator of exposure. Such an indicator could be used to supplement exposure data from workplace air sampling. A biological indicator would be particularly valuable in evaluating workers with intermittent airborne asbestos exposures and in determining if airborne exposure results in penetration through the lung or gastrointestinal tract. Transmission electron microscopy was selected as the most sensitive technique for identification of all sizes of asbestos fibers which might appear in the urine. First morning void urine samples were obtained from six workers (occupationally exposed to chrysotile asbestos in a factory producing roof coatings) and from a control group (six individuals with no occupational exposure). The levels of chrysotile asbestos detected in the urine of five workers were significantly greater than the asbestos concentrations in matched field blanks (both on a number and mass basis). Field blanks were designed to detect asbestos in the urine samples due to contamination which might occur during urine collection. Also, the workers' urinary asbestos levels were significantly greater than the concentrations found in the control group (both on a number and mass basis). Finally, the levels of chrysotile asbestos detected in the urine of two of six controls were significantly greater than those in matched field blanks (both on a number and mass basis). Although the project was not specifically designed to correlate urinary and airborne asbestos concentrations, preliminary data indicated that a correlation did not exist between these factors.