Luminescence of free-standing versus matrix-embedded oxide-passivated silicon nanocrystals: The role of matrix-induced strain:

We collect a large number of experimental data from various sources to demonstrate that free-standing (FS) oxide-passivated silicon nanocrystals (SiNCs) exhibit considerably blueshifted emission, by 200 meV on average, compared to those prepared as matrix-embedded (ME) ones of the same size. This is suggested to arise from compressive strain, exerted on the nanocrystals by their matrix, which plays an important role in the light-emission process; this strain has been neglected up to now as opposed to the impact of quantum confinement or surface passivation. Our conclusion is also supported by the comparison of low-temperature behavior of photoluminescence of matrix-embedded and free-standing silicon nanocrystals

The Effect of Nitrogen Ion Implantation on the Surface Properties of Ti6Al4V Alloy Coated by a Carbon Nanolayer

The ion beam assisted deposition (IBAD) method was chosen for preparing a carbon thin film with a mixing area on a substrate of Ti6Al4V titanium alloy. Nitrogen ions with energy 90 keV were used. These form a broad ion beam mixing area at the interface between the carbon film and the substrate. We investigated the chemical composition by the glow discharge optical emission spectroscopy (GD-OES) method and the phases by the X-ray diffraction (XRD) method. The measured concentration profiles indicate the mixing of the carbon film into the substrate, which may have an effect on increasing the adhesion of the deposited film. The nanohardness and the coefficient of friction were measured. We found that the modified samples had a markedly lower coefficient of friction even after damage to the carbon film, and they also had higher nanohardness than the unmodified samples. The increased nanohardness is attributed to the newly created phases that arose with ion implantation of nitrogen ions

Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor

International audienceAccumulating data support the role of tau pathology in cognitive decline in ageing and Alzheimer's disease, but underlying mechanisms remain ill-defined. Interestingly, ageing and Alzheimer's disease have been associated with an abnormal upregulation of adenosine A2A receptor (A2AR), a fine tuner of synaptic plasticity. However, the link between A2AR signalling and tau pathology has remained largely unexplored. In the present study, we report for the first time a significant upregulation of A2AR in patients suffering from frontotemporal lobar degeneration with the MAPT P301L mutation. To model these alterations, we induced neuronal A2AR upregulation in a tauopathy mouse model (THY-Tau22) using a new conditional strain allowing forebrain overexpression of the receptor. We found that neuronal A2AR upregulation increases tau hyperphosphorylation, potentiating the onset of tau-induced memory deficits. This detrimental effect was linked to a singular microglial signature as revealed by RNA sequencing analysis. In particular, we found that A2AR overexpression in THY-Tau22 mice led to the hippocampal upregulation of C1q complement protein-also observed in patients with frontotemporal lobar degeneration-and correlated with the loss of glutamatergic synapses, likely underlying the observed memory deficits. These data reveal a key impact of overactive neuronal A2AR in the onset of synaptic loss in tauopathies, paving the way for new therapeutic approaches