Catalytic Aspects of Pt/Pd Supported on ZnO Rods for Hydrogen Production in Methanol Steam Reforming

We present a combined experimental and theoretical study for catalytic performance of Pt/Pd supported on ZnO rods for methanol steam reforming reaction (MSR) for hydrogen production. The samples were extensively characterized by Adsorption– Desorption of N2 (BET), electron microscopy in scanning and transmission mode (SEM/TEM), X-ray diffraction (XRD), temperature programed reduction (TPR), and mass spectroscopy (MS). Results, showed typical diffraction peaks corresponding to hexagonal Zincite structure and tetragonal PtZn, PdZn and PtPdZn alloys which were identified by XRD, HRTEM and the last structure by modeling simulation. The crystallographic characterization after catalytic testing indicates that intermetallic PtZn phase on Pt/ZnO sample was more stable in comparison to PdZn on Pd/ZnO catalyst. In addition, Pt stabilize the PdZn structure in the bimetallic catalyst. The catalytic reactivity measured from 200 to 450 °C, indicates that Pt/ZnO-rod sample possess superior catalytic activity from the series as completed on this study. The methanol conversion was tracked by mass spectroscopy concluding minimal changes in outlet signals which suggests samples are chemically stable throughout the complete catalytic reaction. Furthermore, the computer assisted density of states calculations indicate that electron donation from platinum into the zinc oxide support might be the explanation for better catalytic performance

FOXO3 targets are reprogrammed as Huntington's disease neural cells and striatal neurons face senescence with p16INK4a increase.

Neurodegenerative diseases (ND) have been linked to the critical process in aging-cellular senescence. However, the temporal dynamics of cellular senescence in ND conditions is unresolved. Here, we show senescence features develop in human Huntington's disease (HD) neural stem cells (NSCs) and medium spiny neurons (MSNs), including the increase of p16INK4a , a key inducer of cellular senescence. We found that HD NSCs reprogram the transcriptional targets of FOXO3, a major cell survival factor able to repress cell senescence, antagonizing p16INK4a expression via the FOXO3 repression of the transcriptional modulator ETS2. Additionally, p16INK4a promotes cellular senescence features in human HD NSCs and MSNs. These findings suggest that cellular senescence may develop during neuronal differentiation in HD and that the FOXO3-ETS2-p16INK4a axis may be part of molecular responses aimed at mitigating this phenomenon. Our studies identify neuronal differentiation with accelerated aging of neural progenitors and neurons as an alteration that could be linked to NDs

FOXO3 targets are reprogrammed as Huntington's disease neural cells and striatal neurons face senescence with p16 INK4a increase

International audienceNeurodegenerative diseases (ND) have been linked to the critical process in aging-cellular senescence. However, the temporal dynamics of cellular senescence in ND conditions is unresolved. Here, we show senescence features develop in human Huntington's disease (HD) neural stem cells (NSCs) and medium spiny neurons (MSNs), including the increase of p16INK4a , a key inducer of cellular senescence. We found that HD NSCs reprogram the transcriptional targets of FOXO3, a major cell survival factor able to repress cell senescence, antagonizing p16INK4a expression via the FOXO3 repression of the transcriptional modulator ETS2. Additionally, p16INK4a promotes cellular senescence features in human HD NSCs and MSNs. These findings suggest that cellular senescence may develop during neuronal differentiation in HD and that the FOXO3-ETS2-p16INK4a axis may be part of molecular responses aimed at mitigating this phenomenon. Our studies identify neuronal differentiation with accelerated aging of neural progenitors and neurons as an alteration that could be linked to NDs