RESUMO
The A-site cation-ordered GdBa0.5Sr0.5Co2-xCuxO5+δ (GBSCC) double perovskites are evaluated regarding the development of high-performance oxygen electrodes for reversible solid oxide cells (rSOCs). The aims are to maximally decrease the content of toxic and expensive cobalt by substitution with copper while at the same time improving or maintaining the required thermomechanical and electrocatalytic properties. Studies reveal that compositions with 1 ≤ x ≤ 1.15 are particularly interesting. Their thermal and chemical expansions are decreased, and sufficient transport properties are observed. Complementary density functional theory calculations give deeper insight into oxygen defect formation in the considered materials. Chemical compatibility with La0.8Sr0.2Ga0.8Mg0.2O3-δ (LSGM) and Ce0.9Gd0.1O2-δ (GDC) solid electrolytes is evaluated. It is documented that the GdBa0.5Sr0.5Co0.9Cu1.1O5+δ oxygen electrode enables obtaining very low electrode polarization resistance (Rp) values of 0.017 Ω cm2 at 850 °C as well as 0.111 Ω cm2 at 700 °C, which is lower in comparison to that of GdBa0.5Sr0.5CoCuO5+δ (respectively, 0.026 and 0.204 Ω cm2). Systematic distribution of relaxation times analyses allows studies of the electrocatalytic activity and distinguishing elementary steps of the electrochemical reaction at different temperatures. The rate-limiting process is found to be oxygen atom reduction, while the charge transfer at the electrode/electrolyte interface is significantly better with LSGM. The studies also allow elaborating on the catalytic role of the Ag current collector as compared with Pt. The electrodes manufactured using materials with x = 1 and 1.1 permit reaching high power outputs, exceeding 1240 mW cm-2 at 850 °C and 1060 mW cm-2 at 800 °C, for the LSGM-supported cells, which can also work in the electrolysis mode.
RESUMO
Vitamin K (VK) plays many important functions in the body. The most important of them include the contribution in calcium homeostasis and anticoagulation. Vascular calcification (VC) is one of the most important mechanisms of renal pathology. The most potent inhibitor of this process-matrix Gla protein (MGP) is VK-dependent. Chronic kidney disease (CKD) patients, both non-dialysed and hemodialysed, often have VK deficiency. Elevated uncarboxylated matrix Gla protein (ucMGP) levels indirectly reflected VK deficiency and are associated with a higher risk of cardiovascular events in these patients. It has been suggested that VK intake may reduce the VC and related cardiovascular risk. Vitamin K intake has been suggested to reduce VC and the associated cardiovascular risk. The role and possibility of VK supplementation as well as the impact of anticoagulation therapy on VK deficiency in CKD patients is discussed.