development-validation-chromium-getters-for-solid-oxide-fuel-cell

Development and Validation of Chromium Getters for Solid Oxide Fuel Cell Power Systems

Degradation of cathode in solid oxide fuel cells (SOFC) remains a major concern for the long-term performance stability and operational reliability. The ...

University of Connecticut

To validate the Chinese version of the Critical-Care Pain Observation Tool (CPOT) in nonintubated and intubated ICU patients.

Validation of a Chinese version critical-care pain observation tool in nonintubated and intubated critically ill patients: Two cross-sectional studies.

The objective of this study was to evaluate whether fucoxanthin (FCX) have anti-fibrogenic properties in hepatic stellate cells (HSCs). FCX significantly decreased basal and transforming growth factor β1 (TGFβ1)-induced mRNA levels of fibrogenic genes with concomitant decreases in their protein levels in LX-2 cells. The phosphorylation of SMA- and MAD-related protein (SMAD3) was increased by TGFβ1, which was attenuated by FCX. Importantly, when LX-2 cells were treated with FCX and SIS3, a SMAD3 inhibitor, there was synergistic repression of fibrogenic gene expression. The anti-fibrogenic effect of FCX was also confirmed in primary human HSCs. FCX prevented TGFβ1-induced accumulation of reactive oxygen species by diminishing mRNA level of NADPH oxidase 4 (NOX4) in LX-2 cells. When FCX was present during the activation of quiescent mouse primary HSCs, it decreased the expression of fibrogenic genes while diminishing intracellular lipid droplets. The results suggest that FCX exerts an anti-fibrogenic effect in HSCs primarily by preventing TGFβ1-induced pro-fibrogenic genes expression via inhibition of SMAD3 activation and by inhibiting the activation of quiescent HSCs.

Fucoxanthin exerts anti-fibrogenic effects in hepatic stellate cells.

Cells are transplanted to regenerate an organs' parenchyma, but how transplanted parenchymal cells induce stromal regeneration is elusive. Despite the common use of a decellularized matrix, little is known as to the pivotal signals that must be restored for tissue or organ regeneration. We report that Alx3, a developmentally important gene, orchestrated adult parenchymal and stromal regeneration by directly transactivating Wnt3a and vascular endothelial growth factor. In contrast to the modest parenchyma formed by native adult progenitors, Alx3-restored cells in decellularized scaffolds not only produced vascularized stroma that involved vascular endothelial growth factor signalling, but also parenchymal dentin via the Wnt/β-catenin pathway. In an orthotopic large-animal model following parenchyma and stroma ablation, Wnt3a-recruited endogenous cells regenerated neurovascular stroma and differentiated into parenchymal odontoblast-like cells that extended the processes into newly formed dentin with a structure-mechanical equivalency to native dentin. Thus, the Alx3-Wnt3a axis enables postnatal progenitors with a modest innate regenerative capacity to regenerate adult tissues. Depleted signals in the decellularized matrix may be reinstated by a developmentally pivotal gene or corresponding protein.

Boxun Hu

Department of Materials Science and Engineering,
Center for Clean Energy Engineering

University of Connecticut

Development and Validation of Chromium Getters for Solid Oxide Fuel Cell Power Systems

Boxun Hu

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Materials Science and Engineering,Center for Clean Energy Engineering

University of Connecticut

Development and Validation of Chromium Getters for Solid Oxide Fuel Cell Power Systems

Department of Materials Science and Engineering,
Center for Clean Energy Engineering