Electrical characterization of glass-ceramic sealant-metallic interconnect joined samples under solid oxide electrolysis cell conditions; influence on the microstructure and composition at the different polarized interfaces

In this study, the electrical resistivity of a glass-ceramic sealant is evaluated at 850 ◦C, for 2800 h under the applied voltage of 1.6 V. The glass-ceramic sealant is sandwiched between two Crofer22APU plates to produce Crofer22APU/Glass-ceramic/Crofer22APU samples. The Crofer22APU/glass-ceramic/Crofer22APU joints show electrical resistivity around 106-107 Ω cm, significantly high to ensure the insulation between two conductive interconnect plates. The detailed SEM-EDS post mortem analysis showed good thermo-mechanical compatibility of the glass-ceramic with the Crofer22APU substrates, thus excluding any detrimental interaction with the metallic interconnect under high applied voltage. XRD analysis of glass-ceramic confirmed the presence of crystalline phases with suitable CTEs, after electrical resistivity under harsh conditions

Design and characterization of novel glass‐ceramic sealants for solid oxide electrolysis cell (SOEC) applications

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Glass-ceramic sealants for SOEC: Thermal characterization and electrical resistivity in dual atmosphere

A Ba-based glass-ceramic sealant is designed and tested for solid oxide electrolysis cell (SOEC) applications. A suitable SiO2/BaO ratio is chosen in order to obtain BaSi2O5 crystalline phase and subsequently favorable thermo-mechanical properties of the glass-ceramic sealant. The glass is analyzed in terms of thermal, thermo-mechanical, chemical, and electrical behavior. Crofer22APU-sealant-Crofer22APU joined samples are tested for 2000 h at 850 ◦C in a dual atmosphere test rig having reducing atmosphere of H2:H2O 50/50 (mol%) and under the applied voltage of 1.6 V. In order to simulate the SOEC dynamic working conditions, thermal cycles are performed during the long-term electrical resistivity test. The glass-ceramic shows promising behavior in terms of high density, suitable CTE, and stable electrical resistivity (106–107 Ω cm) under SOEC conditions. The SEM-EDS post mortem analysis confirms excellent chemical and thermo-mechanical compatibility of the glass-ceramic with Crofer22APU

Pleural Effusion in a Peritoneal Dialysis Patient

A 34-year-old female presented with end-stage renal disease (ESRD) treated by peritoneal dialysis (CAPD) complained of a dry cough. Chest X-ray and chest computed tomography (CT) scan revealed massive right hydrothorax. Because the glucose concentration of pleural fluid was markedly high compared with that of serum, we performed isotope and contrast peritoneography. We used CT for localizing it. MRI was also trying to show transdiaphragmatic leakage in peritoneoflural fistula. Temporary discontinuation of CAPD, tetracycline instillation into the pleural space and surgical patch grafting of the diaphragmatic leak have all been described. A novel method may be video-assisted talc pleurodesis

Shear performance at room and high temperatures of glass-ceramic sealants for solid oxide electrolysis cell technology

To provide a reliable integration of components within a solid oxide electrolysis cell stack, it is fundamental to evaluate the mechanical properties of the glass-ceramic sealing materials, as well as the stability of the metal-glass-ceramic interface. In this work, the mechanical behavior of two previously developed glass-ceramic sealants joined to Crofer22APU steel is investigated at room temperature, 650 \ub0C, and 850 \ub0C under shear load. The mechanical properties of both the glass-ceramics showed temperature dependence. The shear strength of Crofer22APU/ glass-ceramic/Crofer22APU joints ranged from 14.1 MPa (20 \ub0C) to 1.8 MPa (850 \ub0C). The elastic modulus of both glass-ceramics also reduced with temperature. The volume fraction of the crystalline phases in the glass-ceramics was the key factor for controlling the mechanical properties and fracture, especially above the glass-transition temperature

Mn-Co spinel coatings on Crofer 22 APU by electrophoretic deposition: Up scaling, performance in SOFC stack at 850 °C and compositional modifications

Ceramic coatings for metallic interconnects play a key role in limiting corrosion and chromium evaporation in solid oxide cells. This study presents the upscaling of the electrophoretic deposition (EPD) technique to process Mn-Co spinels on real-dimension Crofer 22 APU interconnects and the test in a SOFC stack. Area specific resistance of long-term test conducted for 5000 h at 850 °C demonstrated that two-steps sintering has a significant influence on the coating performance; an area specific resistance degradation rate of 0.5 mΩ cm2 kh−1 is recorded. Stack test, operated in fuel cell mode at 850 °C for 3000 h under application of 227 mA/cm², including 5 thermal cycles, demonstrated the effectiveness of the electrophoretically deposited Mn-Co spinel in limiting the oxide scale growth on the Crofer 22 APU. An advanced post mortem investigation showed the effectiveness of the EPD ceramic coating, even when considering different and complex surfaces of the Crofer 22 APU

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Objective Marrow-derived endothelial progenitor cells (EPCs) are important in the neovascularization that occurs in diverse conditions such as cardiovascular disorders, inflammatory diseases, and neoplasms. In rheumatoid arthritis (RA), synovial neovascularization propels disease by nourishing the inflamed and hyperproliferative synovium. This study was undertaken to investigate the hypothesis that EPCs selectively home to inflamed joint tissue and may perpetuate synovial neovascularization. Methods In a collagen-induced arthritis (CIA) model, neovascularization and EPC accumulation in mouse ankle synovium was measured. In an antibody-induced arthritis model, EPC recruitment to inflamed synovium was evaluated. In a chimeric SCID mouse/human synovial tissue (ST) model, mice were engrafted subcutaneously with human ST, and EPC homing to grafts was assessed 2 days later. EPC adhesion to RA fibroblasts and RA ST was evaluated in vitro. Results In mice with CIA, cells bearing EPC markers were significantly increased in peripheral blood and accumulated in inflamed synovial pannus. EPCs were 4-fold more numerous in inflamed synovium from mice with anti–type II collagen antibody–induced arthritis versus controls. In SCID mice, EPC homing to RA ST was 3-fold greater than to normal synovium. Antibody neutralization of vascular cell adhesion molecule 1 (VCAM-1) and its ligand component Α4 integrin potently inhibited EPC adhesion to RA fibroblasts and RA ST cryosections. Conclusion These data demonstrate the selective recruitment of EPCs to inflamed joint tissue. The VCAM-1/very late activation antigen 4 adhesive system critically mediates EPC adhesion to cultured RA fibroblasts and to RA ST cryosections. These findings provide evidence of a possible role of EPCs in the synovial neovascularization that is critical to RA pathogenesis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/56042/1/22706_ftp.pd

Circulating Endothelial Progenitor Cells in Kidney Transplant Patients

Background: Kidney transplantation (RTx) leads to amelioration of endothelial function in patients with advanced renal failure. Endothelial progenitor cells (EPCs) may play a key role in this repair process. The aim of this study was to determine the impact of RTx and immunosuppressive therapy on the number of circulating EPCs. Methods: We analyzed 52 RTx patients (58613 years; 33 males, mean 6 SD) and 16 age- and gender-matched subjects with normal kidney function (57617; 10 males). RTx patients received a calcineurin inhibitor (CNI)-based (65%) or a CNI-free therapy (35%) and steroids. EPC number was determined by double positive staining for CD133/VEGFR2 and CD34/VEGFR2 by flow cytometry. Stromal cell-derived factor 1 alpha (SDF-1) levels were assessed by ELISA. Experimentally, to dissociate the impact of RTx from the impact of immunosuppressants, we used the 5/6 nephrectomy model. The animals were treated with a CNI-based or a CNI-free therapy, and EPCs (Sca+cKit+) and CD26+ cells were determined by flow cytometry. Results: Compared to controls, circulating number of CD34+/VEGFR2+ and CD133+/VEGFR2+ EPCs increased in RTx patients. There were no correlations between EPC levels and statin, erythropoietin or use of renin angiotensin system blockers in our study. Indeed, multivariate analysis showed that SDF-1 – a cytokine responsible for EPC mobilization – is independently associated with the EPC number. 5/6 rats presented decreased EPC counts in comparison to control animals. Immunosuppressive therapy was able to restore normal EPC values in 5/6 rats. These effects on EPC number were associated with reduced number of CD26+ cells, which might be related to consequent accumulation of SDF-1. Conclusions: We conclude that kidney transplantation and its associated use of immunosuppressive drugs increases the number of circulating EPCs via the manipulation of the CD26/SDF-1 axis. Increased EPC count may be associated to endothelial repair and function in these patients.

Increased cardiovascular risk in rats with primary renal dysfunction; mediating role for vascular endothelial function

Primary chronic kidney disease is associated with high cardiovascular risk. However, the exact mechanisms behind this cardiorenal interaction remain unclear. We investigated the interaction between heart and kidneys in novel animal model for cardiorenal interaction. Normal Wistar rats and Munich Wistar Fromter rats, spontaneously developing renal dysfunction, were subjected to experimental myocardial infarction to induce cardiac dysfunction (CD) and combined cardiorenal dysfunction (CRD), respectively (N = 5–10). Twelve weeks later, cardiac- and renal parameters were evaluated. Cardiac, but not renal dysfunction was exaggerated in CRD. Accelerated cardiac dysfunction in CRD was indicated by decreased cardiac output (CD 109 ± 10 vs. CRD 79 ± 8 ml/min), diastolic dysfunction (E/e′) (CD 26 ± 2 vs. CRD 50 ± 5) and left ventricular overload (LVEDP CD 10.8 ± 2.8 vs. CRD 21.6 ± 1.7 mmHg). Congestion in CRD was confirmed by increased lung and atrial weights, as well as exaggerated right ventricular hypertrophy. Absence of accelerated renal dysfunction, measured by increased proteinuria, was supported by absence of additional focal glomerulosclerosis or further decline of renal blood flow in CRD. Only advanced peripheral endothelial dysfunction, as found in CRD, appeared to correlate with both renal and cardiac dysfunction parameters. Thus, proteinuric rats with myocardial infarction showed accelerated cardiac but not renal dysfunction. As parameters mimic the cardiorenal syndrome, these rats may provide a clinically relevant model to study increased cardiovascular risk due to renal dysfunction. Peripheral endothelial dysfunction was the only parameter that correlated with both renal and cardiac dysfunction, which may indicate a mediating role in cardiorenal interaction

Cytoprotective pathways in the vascular endothelium. Do they represent a viable therapeutic target?

The vascular endothelium is a critical interface, which separates the organs from the blood and its contents. The endothelium has a wide variety of functions and maintenance of endothelial homeostasis is a multi-dimensional active process, disruption of which has potentially deleterious consequences if not reversed. Vascular injury predisposes to endothelial apoptosis, dysfunction and development of atherosclerosis. Endothelial dysfunction is an end-point, a central feature of which is increased ROS generation, a reduction in endothelial nitric oxide synthase and increased nitric oxide consumption. A dysfunctional endothelium is a common feature of diseases including rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus and chronic renal impairment. The endothelium is endowed with a variety of constitutive and inducible mechanisms that act to minimise injury and facilitate repair. Endothelial cytoprotection can be enhanced by exogenous factors such as vascular endothelial growth factor, prostacyclin and laminar shear stress. Target genes include endothelial nitric oxide synthase, heme oxygenase-1, A20 and anti-apoptotic members of the B cell lymphoma protein-2 family. In light of the importance of endothelial function, and the link between its disruption and the risk of atherothrombosis, interest has focused on therapeutic conditioning and reversal of endothelial dysfunction. A detailed understanding of cytoprotective signalling pathways, their regulation and target genes is now required to identify novel therapeutic targets. The ultimate aim is to add vasculoprotection to current therapeutic strategies for systemic inflammatory diseases, in an attempt to reduce vascular injury and prevent or retard atherogenesis