Estimation of Lubrication Layer Thickness and Composition through Reverse Engineering of Interface Rheometry Tests.

During concrete pumping, a lubrication layer is formed near the pipe wall. Extensive research has been performed on measuring and modeling the properties of this layer and using these values to predict pumping pressures. However, there are numerous discussions in the literature about the composition and thickness of this layer: can it be considered mortar, a micromortar, or is it cement paste? In this paper, possible solutions for the thickness and composition of the lubrication layer are derived from interface rheometry tests. It is assumed that the lubrication layer is composed of one or more concentric layers of paste or micromortar. To accomplish this determination, the rheological properties of the composing paste, mortars with different maximum particle sizes and concrete need to be known. Challenges arising from using different rheometers and from the sensitivity of the paste rheology to shearing are addressed in this contribution. The results show that, mathematically, a single layer of homogeneous paste or mortar with different maximum particle sizes can be responsible for the formation of the lubrication layer. Physically, however, the composing material should contain sand particles to some extent, as particle migration is proportional to the size squared. If the literature results from pumping are applicable to the results obtained in this paper, it seems that the lubrication layer is composed of a mortar with a maximum particle size of around 1 to 2 mm.

Elucidating the Effect of Water-To-Cement Ratio on the Hydration Mechanisms of Cement.

The hydration of cement is often modeled as a phase boundary nucleation and growth (pBNG) process. Classical pBNG models, based on the use of isotropic and constant growth rate of the main hydrate, that is, calcium-silicate-hydrate (C-S-H), are unable to explain the lack of any significant effect of the water-to-cement (w/c) ratio on the hydration kinetics of cement. This paper presents a modified form of the pBNG model, in which the anisotropic growth of C-S-H is allowed to vary in relation to the nonlinear evolution of its supersaturation in solution. Results show that once the supercritical C-S-H nuclei form, their growth remains confined within a region in proximity to the cement particles. This is hypothesized to be a manifestation of the sedimentation of cement particles, which imposes a space constraint for C-S-H growth. In pastes wherein the sedimentation of cement particles is disrupted, the hydration kinetics are no longer unresponsive to changes in w/c. Unlike C-S-H, the ions in solution are not confined, and hence, the supersaturation-dependent growth rate of C-S-H diminishes monotonically with increasing w/c. Overall, the outcomes of this work highlight important aspects that need to be considered in employing pBNG models for simulating hydration of cement-based systems.

Liposomal-delivery of phosphodiesterase 5 inhibitors augments UT-15C-stimulated ATP release from human erythrocytes.

The use of liposomes to affect targeted delivery of pharmaceutical agents to specific sites may result in the reduction of side effects and an increase in drug efficacy. Since liposomes are delivered intravascularly, erythrocytes, which constitute almost half of the volume of blood, are ideal targets for liposomal drug delivery. In vivo, erythrocytes serve not only in the role of oxygen transport but also as participants in the regulation of vascular diameter through the regulated release of the potent vasodilator, adenosine triphosphate (ATP). Unfortunately, erythrocytes of humans with pulmonary arterial hypertension (PAH) do not release ATP in response to the physiological stimulus of exposure to increases in mechanical deformation as would occur when these cells traverse the pulmonary circulation. This defect in erythrocyte physiology has been suggested to contribute to pulmonary hypertension in these individuals. In contrast to deformation, both healthy human and PAH erythrocytes do release ATP in response to incubation with prostacyclin analogs via a well-characterized signaling pathway. Importantly, inhibitors of phosphodiesterase 5 (PDE5) have been shown to significantly increase prostacyclin analog-induced ATP release from human erythrocytes. Here we investigate the hypothesis that targeted delivery of PDE5 inhibitors to human erythrocytes, using a liposomal delivery system, potentiates prostacyclin analog- induced ATP release. The findings are consistent with the hypothesis that directed delivery of this class of drugs to erythrocytes could be a new and important method to augment prostacyclin analog-induced ATP release from these cells. Such an approach could significantly limit side effects of both classes of drugs without compromising their therapeutic effectiveness in diseases such as PAH.