Event-level key changes

Through meticulous splitting of a loop into one or two note events, entirely new melodies can be created with the use of event-level key changes (see Fignre 3.28). While the distortion of snch drastic changes may limit this process somewhat, the increased variety that this process provides makes it possible to avoid the bane of all loop-based music composition—too mucb repetition. 

Set the loop bar to encompass the first four measures and draw an event from a simple bass line in a track in the project. The more simple the bass line is, the easier it is to hear the key changes. At this point, if you also add a basic beat and a piano, the song sounds nearly complete, if a bit boring. Even at tbis very simple level, you can already hear the familiar pop pattern. The project ends up looking like the one illustrated in Figure 3.23. 

FIGURE 14-4. Key components of the pathophysiology of cardiac remodeling. Myocardial injury (e.g., myocardial infarction) results in the activation of a number of hemodynamic and neurohormonal compensatory responses in an attempt to maintain circulatory homeostasis. Chronic activation of the neurohormonal systems results in a cascade of events that affect the myocardium at the molecular and cellular levels. These events lead to the changes in ventricular size, shape, structure, and function known as ventricular remodeling. The alterations in ventricular function result in further deterioration in cardiac systolic and diastolic function, which further promotes the remodeling process. 

The PPARa Activator MOA Is Chemical-Independent. Mode of action is a series of key events that together result in an adverse health effect such as a liver tumor and as such is chemical-independent (Boobis et al. 2008 Holsapple et al. 2006 Meek 2008). Consistent with this the MOA for PPARa activators is an endogenous series of events that can occur independent of chemical exposure. Livers from ACO-nuU mice exhibit severe steatosis, increases in markers of PPARa activation (i.e., genes involved in P- and co-fatty acid oxidation), increases in hydrogen peroxide levels, increases in ceU proliferation and fiver tumors (Fan et al. 1998). The increases in the markers of PPARa were shown to be PPARa-dependent as the changes were abolished in a double ACO-/PPARa-null mouse (Hashimoto et al. 

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