Methane dehydroaromatization was studied over a series of impregnated Mo/ZSM-5 catalysts with different molybdenum contents and Si/Al atomic ratios in the parent H-ZSM-5 zeolites. The maximum catalytic activity (∼14% CH4 conversion) and benzene formation selectivity (∼70%) were observed for the samples with 2%−5% molybdenum. The activity and selectivity are improved when the Si/Al ratio is decreased from 45 to 17. After pretreatment in argon and reaction at 720 °C, the catalysts have been characterized by textural methods, X-ray diffractometry (XRD), differential thermal analysis (DTA), high-resolution transmission electron microscopy (HRTEM), and energy-dispersive X-ray spectroscopy (EDX). As determined by HRTEM, after the pretreatment, the MoO x phase is highly dispersed on the external surface of the zeolite. During the reaction, molybdenum carbide nanoparticles 2−15 nm in size are formed on the external surface, and the molybdenum-containing clusters are deposited in the zeolite channels. The carbonaceous deposits (CDs) are formed as graphite layers on the surface of Mo2C nanoparticles that were >2 nm in size, and as friable layers with a disordered structure on the external surface of the zeolite. According to EDX, XRD, and DTA studies, the content of the CD and the extent of their condensation (the C/H ratio) increase with the time-on-stream. For all the studied molybdenum contents (1%−10%) and time-on-stream values (0.5−6 h), the CDs formed on the catalysts with Si/Al = 17 are characterized by one maximum of the exothermic burn-out effect in DTA, whereas on the catalysts with Si/Al = 30 and 45, they are characterized by two such maxima. A correlation between the catalyst activity, the selectivity versus nanostructure, and the location of the molybdenum phases and CDs is discussed.

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.

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