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The prototype experimental example of "spontaneous" pattern formation in an unstirred chemical medium is the oscillatory Belousov-Zhabotinsky (BZ) reaction: target patterns of outward-moving concentric rings are readily observed when the reaction is run in a thin layer in a Petri dish. In many experimental runs, new target centers appeared to form closer to pre-existing target centers than expected in a randomized model. Here we describe a simple direct test for the presence of temporal order in the spatiotemporal dynamics of target nucleation, and apply this test to detect significant temporal order in target formation in the ferroin-catalyzed BZ reaction. We also describe how mixing heterogeneity can generate temporal order, even in the absence of heterogeneous physical nucleating centers.

The objective of our research was to investigate the effects of the protease inhibitors ritonavir, saquinavir, and indinavir on triglyceride synthesis, lipolysis, insulin binding, and signaling in differentiating 3T3 L1 pre-adipocytes. Saquinavir, ritonavir, and indinavir all stimulated triglyceride (TG) synthesis. Additionally, all concentrations of protease inhibitors employed (i.e., 0.1 micro M to 10 micro M) significantly decreased insulin-stimulated TG synthesis. No effects of any of the protease inhibitors were observed either on basal lipolysis or after stimulation of lipolysis with 100 nM noradrenaline. Specific (125)I-insulin binding was observed to be decreased by exposure to all the protease inhibitors throughout the period of adipocyte phenotype development. This was mediated by indinavir through a receptor decrease and had no effect on receptor affinity. During differentiation with ritonavir (i.e., 1-11 days post addition of differentiating cocktail), insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation was ascertained (day 11) and found to be decreased in the ritonavir exposed cells when compared with control cells. The results reported herein demonstrate protease inhibitor effects on basal TG synthesis while exhibiting decreased insulin-stimulated TG synthesis at physiological concentrations of protease inhibitors. These effects may be subsequent to decreased insulin binding and/or IRS-1 tyrosine phosphorylation.