Continuing development of a computer system (SAAM) for the simulation, analysis, and modeling of bio-kinetic systems. In 1986-1987 yr we advanced the SAAM/CONSAM extensions to allow for increases in the number of compartments, components and adjustable parameters having previously accomplished the increase in the number of data points which can be used with simulator. A """"""""Unix (Ultrix 1.5)"""""""" version of SAAM29/CONSAM was implemented because of the number of users which have chosen to use this operating system and because of the anticipation of the conversion of the Laboratory of Mathematical Biology to this standard operating system. A 30 compartment version of SAAM and CONSAM has been developed using these new tools and is presently being tested for errors. A version of SAAM29 was developed for the UNIX-PC and tested using the previous library of SAAM problems. Because the UNIX-PC functions as both the computer and terminal, software for a virtual terminal was added to CONSAM. The 30+, C-language, subroutines which makeup the virtual terminal utilize the GSS-GKS C bindings. This implementation necessitated the addition of a graph name characteristic to the CONSAM plot command. CONSAM and the virtual terminal are executed as separate independent processes in which information and control can be passed from CONSAM to the virtual terminal on the plot command. The metabolism of human IgE was studied in normals, severe atopics and patients with the hyperimmunoglobulin E-recurrent infection (HIE;Job's) syndrome to understand how IgE metabolism is altered in disorders with marked elevations of serum IgE. Following the development of a new compartmental model for IgE metabolism, it was determined that the fractional catabolic rate for IgE is significantly less for atopic patients (mean plus or minus SEM=0.20 plus or minus 0.01) and for the HIE patients (0.15 plus or minus 0.02) than for the normal volunteers (0.52 plus or minus 0.06; p less than 0.01) and is inversely related (r=-0.851; p less than 0.001) to the serum IgE concentration. Evaluation of these data using the model further lead to a unifying hypothesis of immunoglobulin catabolism.
