Cellulose nanofibrils can be obtained from trees and have considerable potential as a building block for biobased materials. In order to achieve good properties of these materials, the nanostructure must be controlled. Here we present a process combining hydrodynamic alignment with a dispersion–gel transition that produces homogeneous and smooth filaments from a low-concentration dispersion of cellulose nanofibrils in water. The preferential fibril orientation along the filament direction can be controlled by the process parameters. The specific ultimate strength is considerably higher than previously reported filaments made of cellulose nanofibrils. The strength is even in line with the strongest cellulose pulp fibres extracted from wood with the same degree of fibril alignment. Successful nanoscale alignment before gelation demands a proper separation of the timescales involved. Somewhat surprisingly, the device must not be too small if this is to be achieved.

Extracorporeal membrane oxygenation (ECMO) is used for rescue in severe respiratory and/or circulatory failure. The patient’s blood is pumped over artificial surfaces in the ECMO circuit. A platelet activation model was applied to study the potential thrombogenicity of ECMO circuit components: the centrifugal blood pump, cannulae, and tubing connectors. Based on the accumulated effect of the scalar form of the stress acting on the platelet over time, the activation model enables assessment of platelet activation and pinpoints regions of elevated activation risk in a component. Numerical simulations of the flow in different components of the ECMO circuit was carried out where the activation level is a function of the impact of local stress and its history along the path that the platelets follow. The results showed that the pump carried the largest risk for platelet activation followed by the reinfusion cannula and lastly the connectors. Pump thrombogenicity was mainly due to long residence time and high shear-rate while the connector showed a high level of non-stationary shear-rate that in turn may contribute to the formation of aggregates through direct platelet activation or through high shear-rate modulation of the vWF multimers.

Complex, unsteady fluid flow phenomena in the arteries arise due to the pulsations of the heart that intermittently pumps the blood to the extremities of the body. The many different flow waveform variations observed throughout the arterial network are a result of this process and a function of the vessel properties. Large scale secondary flow structures are generated throughout the aortic arch and larger branches of the arteries. An experimental 180° curved artery test section with physiological inflow conditions was used to validate the computational methods implemented in this study. Good agreement of the secondary flow structures is obtained between experimental and numerical studies of a Newtonian blood-analog fluid under steady-state and pulsatile, carotid artery flow rate waveforms. Multiple vortical structures, some of opposite rotational sense to Dean vortices, similar to Lyne-type vortices, were observed to form during the systolic portion of the pulse. Computational tools were used to assess the effect of blood-analog fluid rheology (i.e., Newtonian versus non-Newtonian). It is demonstrated that non-Newtonian, blood-analog fluid rheology results in shear layer instabilities that alter the formation of vortical structures during the systolic deceleration and onwards during diastole. Additional vortices not observed in the Newtonian cases appear at the inside and outside of the bend at various times during the pulsation. The influence of blood-analog shear-thinning viscosity decreases mean pressure losses in contrast to the Newtonian blood analog fluid.