Passive pumping using gravity-driven flow is a fascinating approach for microfluidic systems. When designing a passive pumping system, generated flow rates should be known precisely. While reported models used to estimate the flow rates do not usually consider capillary forces, this paper shows that their exclusion is unrealistic in typical gravity-driven systems. Therefore, we propose a new analytical model to estimate the generated flow rates. An extensive set of measurements is used to verify that the proposed model provides a remarkably more precise approximation of the real flow rates compared to the previous models. It is suggested that the developed model should be used when designing a gravity-driven pumping system.
C-CNFs were used as an aid to disperse CNTs, and additional c-CNFs guided the self-assembly between nanocomponents resulting in a nanocomposite film with anisotropic properties.
Ischemic heart disease (IHD) is one of the leading causes of mortality worldwide. Preserving functionality and preventing arrhythmias of the heart are key principles in the management of patients with IHD. Levosimendan, a unique calcium (Ca2+) enhancer with inotropic activity, has been introduced into clinical usage for heart failure treatment. Human-induced pluripotent cell-derived cardiomyocytes (hiPSC-CMs) offer an opportunity to better understand the pathophysiological mechanisms of the disease as well as to serve as a platform for drug screening. Here, we developed an in vitro IHD model using hiPSC-CMs in hypoxic conditions and defined the effects of the subsequent hypoxic stress on CMs functionality. Furthermore, the effect of levosimendan on hiPSC-CMs functionality was evaluated during and after hypoxic stress. The morphology, contractile, Ca2+-handling, and gene expression properties of hiPSC-CMs were investigated in response to hypoxia. Hypoxia resulted in significant cardiac arrhythmia and decreased Ca2+ transient amplitude. In addition, disorganization of sarcomere structure was observed after hypoxia induction. Interestingly, levosimendan presented significant antiarrhythmic properties, as the arrhythmia was abolished or markedly reduced with levosimendan treatment either during or after the hypoxic stress. Moreover, levosimendan presented significant protection from the sarcomere alterations induced by hypoxia. In conclusion, this chip model appears to be a suitable preclinical representation of IHD. With this hypoxia platform, detailed knowledge of the disease pathophysiology can be obtained. The antiarrhythmic effect of levosimendan was clearly observed, suggesting a possible new clinical use for the drug.