An association between high serum calcium/phosphate and cardiovascular events or death is well-established. However, a mechanistic explanation of this correlation is lacking. Here, we examined the role of calciprotein particles (CPPs), nanoscale bodies forming in the human blood upon its supersaturation with calcium and phosphate, in cardiovascular disease. The serum of patients with coronary artery disease or cerebrovascular disease displayed an increased propensity to form CPPs in combination with elevated ionised calcium as well as reduced albumin levels, altogether indicative of reduced Ca2+-binding capacity. Intravenous administration of CPPs to normolipidemic and normotensive Wistar rats provoked intimal hyperplasia and adventitial/perivascular inflammation in both balloon-injured and intact aortas in the absence of other cardiovascular risk factors. Upon the addition to primary human arterial endothelial cells, CPPs induced lysosome-dependent cell death, promoted the release of pro-inflammatory cytokines, stimulated leukocyte adhesion, and triggered endothelial-to-mesenchymal transition. We concluded that CPPs, which are formed in the blood as a result of altered mineral homeostasis, cause endothelial dysfunction and vascular inflammation, thereby contributing to the development of cardiovascular disease.

No abstract

It has been established, that proton-exchanged LiNbO3 waveguides have a marked subsurface layer with structural disorder inducing degradation of electro-optical properties of these waveguides. At the same time, such a subsurface disorder is found to be less pronounced in soft proton-exchanged (SPE) waveguides in comparison with annealed proton-exchanged (APE) ones. The experimental samples of phase modulators fabricated by SPE technique exhibit a better electro-optical efficiency compared to the LiNbO3 modulators produced by the standard and improved APE techniques.

No abstract

No abstract