It is known that the oscillations involve intracellular calcium and activation of the Rho pathway, which occurs following microtubule depolymerization. In a previous study , we used CMAP to propose a mechanism for the generation of cortical oscillations that involved a negative feedback loop in which myosin-based contractility negatively regulated stretch activated calcium channels. The SACs opened due to stretching of the cell surface when the cytosol moves from one side of the cell to the other. The combination of PAGE and DAPI staining represents a rapid, easy and widely available method to the evaluation of inositol pyrophosphates. Here, we used this method to study IP6K1 and Vip1 enzymatic reactions, revealing the existence of a number of additional, previously uncharacterised pyrophosphorylated inositol species. More importantly, parallel analyses comparing SAX-HPLC- and PAGE-based methods reveal a significant underestimation of the quantity and composition of inositol pyrophosphate metabolism. Inositol pyrophosphates are typically subjected to acidic conditions before and during SAX-HPLC analysis. The study of these treatments using PAGE revealed the degrading effects of such actions. TZD inhibits VSMC proliferation and migration through the activation of PPARc, which tends to inhibit the expression of several genes involved in ERK-dependent mitogenic response, leading to the inhibition of cell growth and, finally, cell migration. This peptide, also called FX06, was shown to prevent myocardial reperfusion injury and to reduce infarct sizes in animal models for myocardial ischemia/reperfusion. Also in a multi-centre phase IIa clinical trial FX06 significantly reduced the size of the necrotic core of infarcts in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Parts of this beneficial effect may be explained by the antiinflammatory properties of FX06. With PCI-32765 VE-cadherin being the molecular target of FX06 we wished to test the hypothesis that this peptide is also interfering with endothelial barrier function. Then we apply hypotheses generation to the problem of cortical oscillations of spreading cells. Our goal is to develop a tool to investigate the behavior of living systems and to provide substantial guidance to experimentalists. We therefore selected two different models for capillary leak. First, we used an animal model for Dengue shock syndrome. Given that PGC-1a acts as a transcriptional coactivator for PPARc, thus regulating many physiological processes , we hypothesized that the downregulation of PGC-1a by glucose may play a role in an in vitro-model of VSMC proliferation and migration induced by hyperglycemia. Our results show that overexpression of PGC-1a by adenoviral infection abolishes , while suppression of PGC-1a amplifies hyperglycemia-induced VSMC proliferation and migration, providing evidence for a direct role of PGC-1a in this process.