Finally, platelet activating factor, a lipid mediator generated after eosinophil stimulation, induces the activation of platelets, leukocytes and endothelial cells. It would be interesting to determine if the increase of TF observed in eosinophils of patients with hypereosinophilia occurs primarily inside the cell or at transmembrane level. The latter possibility could be relevant to the increase of thrombotic risk due to the interaction of transmembrane TF with the other blood components. Our results do not allow to distinguish between intracellular and transmembrane TF since the antibody used recognizes the extracellular domain of TF which is shared by the two forms. Thus, to define the subcellular localization of TF in hypereosinophilic conditions further methods are needed using the approach of Moosbauer et al. with electronic microscopy or that of Mandal et al. and Pen?a et al. with confocal microscopy. Some hypereosinophilic conditions such as idiopathic hypereosinophilic syndrome, Churg-Strauss syndrome and bullous pemphigoid are characterized by an increased incidence of thrombotic events. It is conceivable that TF expression by eosinophils has an important role in increasing the thrombotic risk of patients with hypereosinophilic conditions. Although the amount of TF generated by and stored in peripheral blood eosinophils is variable and may be small or moderate compared to other cell types, the presence of large numbers of eosinophils in hypereosinophilic conditions may markedly amplify the TF effect on Diacerein coagulation. The observation that two of our patients with idiopathic hypereosinophilic syndrome experienced ischemic heart attacks, healed after steroid-induced normalization of the eosinophil count, further supports a link between eosinophils and cardiovascular events. In recent years, a variety of in vitro 3D cell culture methods have been designed to study either the interaction of multiple cell types or the effect of certain drugs on tissue- or organ-specific microarchitecture. Advances in microfabrication and polymer processing technologies have enabled the development of highly complex systems where a variety of cell types can be cocultured in a controlled environment, thereby establishing a new multidisciplinary scientific field known as organ on a chip. Organ on a chip devices have been Homatropine Bromide developed to study the pathophysiology of a variety of organs, including lung, liver, gut and kidney. The main interest in developing such systems is to culture cells under real world conditions. For that, microfluidic structures allowing cell stimulation with culture media are needed. This is especially relevant when analyzing the behavior of endothelial cells which are continuously stimulated by blood flow-derived shear stress inside the human body. Therefore, shear stress must be applied over cultured endothelium in order to mimic the cell behavior in human vascular systems. The liver, in particular, has attracted much of the research in organ on a chip due to its central role in drug metabolism, toxicity control, and the impact of clinical diseases. In order to properly study the pathophysiology of liver diseases, the unique hepatic microcirculatory architecture should be considered. The liver sinusoid, mainly composed by endothelial cells and stellate cells, plays an essential role in most liver diseases since it represents the sieve plate by which oxygen and nutrients, but also toxicants 
and viruses, enter the parenchyma. In the specific scenario of liver cirrhosis, the hepatic sinusoid is considered a major contributor to the progression, aggravation, and also regression upon treatment of cirrhosis. Phenotypic changes in sinusoidal cells lead to deregulated paracrine interactions that markedly.