Our current disease progression model depends on two parameters. The first is the age of onset, at which calcified zones are first added to the model. Second, we assume a simple growth law for the calcific nodules: the boundary is allowed to spread outward at a constant speed. This speed, the growth rate, is the other parameter. We ran our model with onset ages from 40 to 70 years and growth rates from 0.25 mm/year to 1.0 mm/year. The growth rates were chosen to reflect the observed number of years required for calcification to progress fully across the cusp, from onset to valve failure. The percentage of the total leaflet area that is covered by calcification is plotted versus time in Figure 4 given a constant growth rate of 1 mm/year. With the boundary moving at a constant speed, the calcified area increases quadratically before saturating when the whole leaflet is covered. For each age of onset, the valve was simulated with each rate once for 6-Chloropurine every year until the model valve was entirely calcified. A number of measures of overall valve function and progression of valvular disease have been suggested, including peak fluid velocity, pressure drop across valve, effective orifice area, valve resistance, energy loss, rate of change in valve area, and others. To track the overall valve function over time in our simulations, we calculate the peak fluid velocity and aortic valve opening area at each age. Additionally, the area is an intrinsic measure of valve function, relatively insensitive to varying boundary conditions. The peak velocity for each simulation is simply the maximum fluid velocity in the simulated cardiac cycle. AVA for each simulation is the maximum value of the area calculated throughout the cardiac cycle using the Gorlin formula. Simulation results were compared to experimental data for a typical case of valve aging with CAS. Piper et al, 2004 gives experimentally-derived functions for AVA versus age given the calcification state of the valve at one point in time. We compared our predicted AVA to the experimentally-determined curve for a valve which is unobstructed until onset of calcification at age 50. We also compared our predicted peak velocities to a curve calculated from the experimental AVA by the Gorlin formula. The ability to mount an inflammatory response following injury or exposure to foreign organisms is vital for host homeostasis and survival. However, a persistently heightened immune response such as that observed in chronic inflammatory disorders severely impairs host organ function,Linaclotide ultimately resulting in disease. A major risk associated with chronic inflammation is increased likelihood of cancer development. This uncontrolled immune response likely represents a defect in one or more immunosuppressive mechanisms intended to provide tolerance to the host intestinal microbiota, resulting in the over-production of proinflammatory mediators. The human colon harbor’s as many as 36,000 bacterial species amounting to over 100 trillion aerobic and anaerobic bacteria. As a product of our co-evolution with bacteria, a communication system has developed that allow us to regulate one another, thereby maintaining intestinal homeostasis.