They still tended to migrate to the pole, though the quasi-steady location was more variable; with higher interaction energy, seeds formed more frequently, and there were more granules forming at non-pole locations. The periplasm at the cell poles is a favored place for localization. It has been demonstrated that GFP expressed in the periplasm relocates to the pole when subjected to a mild osmotic shock. The osmotic shock provides a mechanical force to propel GFP proteins into the energetically more favorable location. GFP is huge compared to the narrow periplasmic space. The periplasm is also full of biological ‘gel’ and the diffusion coefficient of GFP in the periplasm has been measured as 2.6 mm2 /s, much lower than in cytoplasm. A formazan molecule, that is about 155 times smaller than GFP and its small aggregates would diffuse more readily towards the pole. Our computer simulation indicated that the experimentally observed granule localization could be obtained only if the TTC reduction rate was slower than the time requires for a seed to defuse from midcell to the pole. It is worth noting that the TTC reduction in E. coli cells is slow. Under fast growth conditions, the granule-containing cells were hard to analyze due to the dilution effect of cell division. To roughly estimate the reduction rate in periplasm, we measured six BU 4061T largest granule cutting surfaces on the ultrathin sections of cells growing for 2 h, 4 h, and 6 h in the presence of TTC. The granule volume was estimated as a 10-mm-thick flat sheet, because membrane deformation did not occur up to 12-h incubation. This result indicated that a granule needs,10 s to grow large enough to be trapped in the periplasm and the cell reduced one TTC molecule per 6 ms, much longer than the time needed for them to diffuse to the pole. The simulation also indicated that high reduction rate would enhance the non-pole localization of granules. We increased the reduction rate by adding more TTC into the medium. As expected, the number of non-pole granules and the number of multiplegranule cells increased when more TTC was supplemented. Endothelial cells are subjected to blood-flow generated laminar shear stress. The laminar flow in blood vessels is pulsatile and can reach shear stress levels of 10 to 70 dyne/cm2. High shear stress induces an atheroprotective endothelial phenotype while absence of shear stress, as occurs near bends and at bifurcations, leads to endothelial dysfunction, characterized by a reduction in barrier function and upregulation of pro-inflammatory gene expression. These sites of disturbed blood flow are more prone to atherosclerotic lesion development. It is well-established that hemodynamic forces have a considerable impact on vascular ECs. One of the transcription factors that are induced by hemodynamic forces is Kru¨ppel-like factor 2, which was found to be absent from atheroprone vascular regions and may be considered atheroprotective. Increased expression of KLF2 is also induced by 3-hydroxy-3- methyl-glutaryl-CoA reductase inhibitors while inflammatory cytokin.