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The upconversion quantum yield (UCQY) is one of the most significant parameters for upconverter materials. A high UCQY is essential for a succesful integration of upconversion in many applications, such as harvesting of the solar radiation. However, little is known about which doping level of the rare-earth ions yields the highest UCQY in the different host lattices and what are the underlying causes. Here, we investigate which Er 3+ doping yields the highest UCQY in the host lattices β-NaYF 4 and Gd 2 O 2 S under 4 I 15/2 → 4 I 13/2 excitation. We show for both host lattices that the optimum Er 3+ doping is not fixed and it actually decreases as the irradiance of the excitation increases. To find the optimum Er 3+ doping for a given irradiance, we determined the peak position of the internal UCQY as a function of the average Er−Er distance. For this purpose, we used a fit on experimental data, where the average Er−Er distance was calculated from the Er 3+ doping of the upconverter samples and the lattice parameters of the host materials. We observe optimum average Er−Er distances for the host lattices β-NaYF 4 and Gd 2 O 2 S with differences <14% at the same irradiance levels, whereas the optimum Er 3+ doping are around 2× higher for β-NaYF 4 than for Gd 2 O 2 S. Estimations by extrapolation to higher irradiances indicate that the optimum average Er−Er distance converges to values around 0.88 and 0.83 nm for β-NaYF 4 and Gd 2 O 2 S, respectively. Our findings point to a fundamental relationship and focusing on the average distance between the active rare-earth ions might be a very efficient way to optimize the doping of rareearth ions with regard to the highest achievable UCQY.

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Sickle cell trait, a common hereditary blood disorder, protects carriers from severe disease in infections with the human malaria parasite Plasmodium falciparum. Protection is associated with a reduced capacity of parasitized erythrocytes to cytoadhere to the microvascular endothelium and cause vaso-occlusive events. However, the underpinning cellular and biomechanical processes are only partly understood and the impact on endothelial cell activation is unclear. Here, we show, by combining quantitative flow chamber experiments with multiscale computer simulations of deformable cells in hydrodynamic flow, that parasitized erythrocytes containing the sickle cell haemoglobin displayed altered adhesion dynamics, resulting in restricted contact footprints on the endothelium. Main determinants were cell shape, knob density and membrane bending. As a consequence, the extent of endothelial cell activation was decreased. Our findings provide a quantitative understanding of how the sickle cell trait affects the dynamic cytoadhesion behavior of parasitized erythrocytes and, in turn, endothelial cell activation.