The motivation for this study was to develop a microdevice for the precise rheological characterization of biofluids, especially blood. The method presented was based on the principles of rheometry and fluid mechanics at the microscale. Traditional rheometers require a considerable amount of space, are expensive, and require a large volume of sample. A mathematical model was developed that, combined with a proper experimental model, allowed us to characterize the viscosity of Newtonian and non-Newtonian fluids at different shear rates. The technology presented here is the basis of a point-of-care device capable of describing the nonlinear rheology of biofluids by the fluid/air interface front velocity characterization through a microchannel. The proposed microrheometer uses a small amount of sample to deliver fast and accurate results, without needing a large laboratory space. Blood samples from healthy donors at distinct hematocrit percentages were the non-Newtonian fluid selected for the study. Water and plasma were employed as testing Newtonian fluids for validation of the system. The viscosity results obtained for the Newtonian and non-Newtonian fluids were consistent with pertinent studies cited in this paper. In addition, the results achieved using the proposed method allowed distinguishing between blood samples with different characteristics.

Combining single cell experiments, population dynamics and theoretical methods of membrane mechanics, we put forward that the rate of cell proliferation in E. coli colonies can be regulated by modifiers of the mechanical properties of the bacterial membrane. Bacterial proliferation was modelled as mediated by cell division through a membrane constriction divisome based on FtsZ, a mechanically competent protein at elastic interaction against membrane rigidity. Using membrane fluctuation spectroscopy in the single cells, we revealed either membrane stiffening when considering hydrophobic long chain fatty substances, or membrane softening if short-chained hydrophilic molecules are used. Membrane stiffeners caused hindered growth under normal division in the microbial cultures, as expected for membrane rigidification. Membrane softeners, however, altered regular cell division causing persistent microbes that abnormally grow as long filamentous cells proliferating apparently faster. We invoke the concept of effective growth rate under the assumption of a heterogeneous population structure composed by distinguishable individuals with different FtsZ-content leading the possible forms of cell proliferation, from regular division in two normal daughters to continuous growing filamentation and budding. The results settle altogether into a master plot that captures a universal scaling between membrane rigidity and the divisional instability mediated by FtsZ at the onset of membrane constriction.

We study the time evolution of the shape of a vesicle membrane under time-dependent spontaneous curvature by means of phase-field model. We introduce the variation in time of the spontaneous curvature via a second field which represents the concentration of a substance that anchors with the lipid bilayer thus changing the local curvature and producing constriction. This constriction is mediated by the action on the membrane of an structure resembling the role of a Z ring. Our phase-field model is able to reproduce a number of different shapes that have been experimentally observed. Different shapes are associated with different constraints imposed upon the model regarding conservation of membrane area. In particular, we show that if area is conserved our model reproduces the so-called L-form shape. By contrast, if the area of the membrane is allowed to grow, our model reproduces the formation of a septum in the vicinity of the constriction. Furthermore, we propose a new term in the free energy which allows the membrane to evolve towards eventual pinching.

The spleen is a hematopoietic organ that participates in cellular and humoral immunity. It also serves as a quality control mechanism for removing senescent and/or poorly deformable red blood cells (RBCs) from circulation. Pitting is a specialized process by which the spleen extracts particles, including malaria parasites, from within circulating RBCs during their passage through the interendothelial slits (IES) in the splenic cords. To study this physiological function in vitro, we have developed two microfluidic devices modeling the IES, according to the hypothesis that at a certain range of mechanical stress on the RBC, regulated through both slit size and blood flow, would force it undergo the pitting process without affecting the cell integrity. To prove its functionality in replicating pitting of malaria parasites, we have performed a characterization of P. falciparum -infected RBCs (P.f. -RBCs) after their passage through the devices, determining hemolysis and the proportion of once-infected RBCs (O-iRBCs), defined by the presence of a parasite antigen and absence of DAPI staining of parasite DNA using a flow cytometry-based approach. The passage of P.f. -RBCs through the devices at the physiological flow rate did not affect cell integrity and resulted in an increase of the frequency of O-iRBCs. Both microfluidic device models were capable to replicate the pitting of P.f. -RBCs ex vivo by means of mechanical constraints without cellular involvement, shedding new insights on the role of the spleen in the pathophysiology of malaria.