Development and Characterization of Size-controlled Non-spherical Platinum Nanoparticles as Catalyst for Proton Exchange Membrane Fuel Cells

Platinum (Pt) nanoparticles with different sizes of 2nm and 5nm supported on functionalized high surface area carbon (HSC) have been successfully synthesized with a one-pot synthesis technique in large scale. Of the interest for the proton exchange membrane fuel cell applications, the synthesized supported catalysts are evaluated by physical characterizations, half-cell and scaled up single cell tests to study the impact of the catalyst sizes on cell performance and durability. Physical characterizations clearly demonstrate the sizes, shapes, crystallinity phases, and the total loading of the Pt nanoparticles on HSC. Half cell characterizations demonstrate higher electrochemical surface area, higher mass activity, and less durability for the working electrode prepared by the smaller Pt nanoparticle sizes (2nm) than the larger Pt nanoparticles (5nm). Scaled up single cell tests using air and hydrogen as the cathode and anode reactants demonstrate the membrane electrode assembly (MEA) prepared by smaller Pt nanoparticle sizes (2nm) shows the maximum power density of 1.1 W/cm2, which is 7% higher than the maximum power density of MEA prepared by larger Pt nanoparticles (5nm) under similar operational conditions. The 30,000 cycles of accelerated stress test on the membrane electrode assembly prepared by larger Pt nanoparticles (5nm) demonstrates 13% drop at maximum power density, illustrating the excellent performance against degradation (ageing)

Hemiballism-hemichorea induced by ketotic hyperglycemia: case report with PET study and review of the literature

Hemiballism-hemichorea (HB-HC) is commonly used to describe the basal ganglion dysfunction in non-ketotic hyperglycemic elderly patients. Here we report two elderly female patients with acute onset of involuntary movements induced by hyperglycemia with positive urine ketones. We described the computed tomography and magnetic resonance imaging findings in these two patients, which is similar to that of non-ketotic hyperglycemic HB-HC patients. FDG-PET was performed and the glucose metabolism in the corresponding lesion in these two patients was contradictory with each other. We tried to clarify the underlying mechanisms of HB-HC and explain the contradictory neuroradiological findings in FDG-PET as being performed at different clinical stages

The effect of non-spherical platinum nanoparticle sizes on the performance and durability of proton exchange membrane fuel cells

Platinum (Pt) nanoparticles with different sizes of 2 nm and 5 nm supported on functionalized high surface area carbon (HSC) have been successfully synthesized with a one-pot synthesis technique in large scale. Of the interest for the proton exchange membrane fuel cell applications, the synthesized supported catalysts are evaluated by physical characterizations, half-cell and scaled up single cell tests to study the impact of the catalyst sizes on cell performance and durability. Physical characterizations clearly demonstrate the sizes, shapes, crystallinity phases, and the total loading of the Pt nanoparticles on HSC. Half cell characterizations demonstrate higher electrochemical surface area, higher mass activity, and less durability for the working electrode prepared by the smaller Pt nanoparticle sizes (2 nm) than the larger Pt nanoparticles (5 nm). Scaled up single cell tests using air and hydrogen as the cathode and anode reactants demonstrate the membrane electrode assembly (MEA) prepared by smaller Pt nanoparticle sizes (2 nm) shows the maximum power density of 1.1 W/cm2, which is 7% higher than the maximum power density of MEA prepared by larger Pt nanoparticles (5 nm) under similar operational conditions. The 30,000 cycles of accelerated stress test on the membrane electrode assembly prepared by larger Pt nanoparticles (5 nm) demonstrates 13% drop at maximum power density, illustrating the excellent performance against degradation (ageing).Canadian Urban Transit Research and Innovation Consortium || Natural Sciences and Engineering Research Council of Canad

Inhibition of nitric oxide in LPS-stimulated macrophages of young and senescent mice by δ-tocotrienol and quercetin

Abstract Background Changes in immune function believed to contribute to a variety of age-related diseases have been associated with increased production of nitric oxide (NO). We have recently reported that proteasome inhibitors (dexamethasone, mevinolin, quercetin, δ-tocotrienol, and riboflavin) can inhibit lipopolysaccharide (LPS)-induced NO production in vitro by RAW 264.7 cells and by thioglycolate-elicited peritoneal macrophages derived from four strains of mice (C57BL/6, BALB/c, LMP7/MECL-1-/- and PPAR-α-/- knockout mice). The present study was carried out in order to further explore the potential effects of diet supplementation with naturally-occurring inhibitors (δ-tocotrienol and quercetin) on LPS-stimulated production of NO, TNF-α, and other pro-inflammatory cytokines involved in the ageing process. Young (4-week-old) and senescent mice (42-week old) were fed control diet with or without quercetin (100 ppm), δ-tocotrienol (100 ppm), or dexamethasone (10 ppm; included as positive control for suppression of inflammation) for 4 weeks. At the end of feeding period, thioglycolate-elicited peritoneal macrophages were collected, stimulated with LPS, LPS plus interferon-β (IFN-β), or LPS plus interferon-γ (IFN-γ), and inflammatory responses assessed as measured by production of NO and TNF-α, mRNA reduction for TNF-α, and iNOS genes, and microarray analysis. Results Thioglycolate-elicited peritoneal macrophages prepared after four weeks of feeding, and then challenged with LPS (10 ng or 100 ng) resulted in increases of 55% and 73%, respectively in the production of NO of 46-week-old compared to 8-week-old mice fed control diet alone (respective control groups), without affecting the secretion of TNF-α among these two groups. However, macrophages obtained after feeding with quercetin, δ-tocotrienol, and dexamethasone significantly inhibited (30% to 60%; P < 0.02) the LPS-stimulated NO production, compared to respective control groups. There was a 2-fold increase in the production of NO, when LPS-stimulated macrophages of quercetin, δ-tocotrienol, or dexamethasone were also treated with IFN-β or IFN-γ compared to respective control groups. We also demonstrated that NO levels and iNOS mRNA expression levels were significantly higher in LPS-stimulated macrophages from senescent (0.69 vs 0.41; P < 0.05), compared to young mice. In contrast, age did not appear to impact levels of TNF-α protein or mRNA expression levels (0.38 vs 0.35) in LPS-stimulated macrophages. The histological analyses of livers of control groups showed lesions of peliosis and microvesicular steatosis, and treated groups showed Councilman body, and small or large lymphoplasmacytic clusters. Conclusions The present results demonstrated that quercetin and δ-tocotrienols inhibit the LPS-induced NO production in vivo. The microarray DNA analyses, followed by pathway analyses indicated that quercetin or δ-tocotrienol inhibit several LPS-induced expression of several ageing and pro-inflammatory genes (IL-1β, IL-1α, IL-6, TNF-α, IL-12, iNOS, VCAM1, ICAM1, COX2, IL-1RA, TRAF1 and CD40). The NF-κB pathway regulates the production of NO and inhibits the pro-inflammatory cytokines involved in normal and ageing process. These ex vivo results confirmed the earlier in vitro findings. The present findings of inhibition of NO production by quercetin and δ-tocotrienol may be of clinical significance treating several inflammatory diseases, including ageing process.Peer Reviewe

Suppression of nitric oxide induction and pro-inflammatory cytokines by novel proteasome inhibitors in various experimental models

<p>Abstract</p> <p>Background</p> <p>Inflammation has been implicated in a variety of diseases associated with ageing, including cancer, cardiovascular, and neurologic diseases. We have recently established that the proteasome is a pivotal regulator of inflammation, which modulates the induction of inflammatory mediators such as TNF-α, IL-1, IL-6, and nitric oxide (NO) in response to a variety of stimuli. The present study was undertaken to identify non-toxic proteasome inhibitors with the expectation that these compounds could potentially suppress the production of inflammatory mediators in ageing humans, thereby decreasing the risk of developing ageing related diseases. We evaluated the capacity of various proteasome inhibitors to suppress TNF-α, NO and gene suppression of TNF-α, and iNOS mRNA, by LPS-stimulated macrophages from several sources. Further, we evaluated the mechanisms by which these agents suppress secretion of TNF-α, and NO production. Over the course of these studies, we measured the effects of various proteasome inhibitors on the RAW 264.7 cells, and peritoneal macrophages from four different strains of mice (C57BL/6, BALB/c, proteasome double subunits knockout LMP7/MECL-1^-/-, and peroxisome proliferator-activated receptor-α,^-/-(PPAR-α,^-/-) knockout mice. We also directly measured the effect of these proteasome inhibitors on proteolytic activity of 20S rabbit muscle proteasomes.</p> <p>Results</p> <p>There was significant reduction of chymotrypsin-like activity of the 20S rabbit muscle proteasomes with dexamethasone (31%), mevinolin (19%), δ-tocotrienol (28%), riboflavin (34%), and quercetin (45%; <b><it>P </it></b>< 0.05). Moreover, quercetin, riboflavin, and δ-tocotrienol also inhibited chymotrypsin-like, trypsin-like and post-glutamase activities in RAW 264.7 whole cells. These compounds also inhibited LPS-stimulated NO production and TNF-α, secretion, blocked the degradation of P-IκB protein, and decreased activation of NF-κB, in RAW 264.7 cells. All proteasome inhibitors tested also significantly inhibited NO production (30% to 60% reduction) by LPS-induced thioglycolate-elicited peritoneal macrophages derived from all four strains of mice. All five compounds also suppressed LPS-induced TNF-α, secretion by macrophages from C57BL/6 and BALB/c mice. TNF-α, secretion, however, was not suppressed by any of the three proteasome inhibitors tested (δ-tocotrienol, riboflavin, and quercetin) with LPS-induced macrophages from LMP7/MECL-1^-/-and PPAR-α,^-/-knockout mice. Results of gene expression studies for TNF-α, and iNOS were generally consistent with results obtained for TNF-α, protein and NO production observed with four strains of mice.</p> <p>Conclusions</p> <p>Results of the current study demonstrate that δ-tocotrienol, riboflavin, and quercetin inhibit NO production by LPS-stimulated macrophages of all four strains of mice, and TNF-α, secretion only by LPS-stimulated macrophages of C57BL/6 and BALB/c mice. The mechanism for this inhibition appears to be decreased proteolytic degradation of P-IκB protein by the inhibited proteasome, resulting in decreased translocation of activated NF-κB to the nucleus, and depressed transcription of gene expression of TNF-α, and iNOS. Further, these naturally-occurring proteasome inhibitors tested appear to be relatively potent inhibitors of multiple proteasome subunits in inflammatory proteasomes. Consequently, these agents could potentially suppress the production of inflammatory mediators in ageing humans, thereby decreasing the risk of developing a variety of ageing related diseases.</p

Rapid Determination of Nine Acrylates in Food Contact Materials by Ultra Performance Convergence Chromatography

Ultra performance convergence chromatography (UPC2) was used to establish a rapid analytical method to determine nine acrylate compounds in plastic food contact materials simultaneously. The samples were extracted with methanol, filtered through an organic membrane, and separated on an ACQUITY UPC2 HSS C18 SB column with gradient elution using a mobile phase consisting of supercritical carbon dioxide and acetonitrile. The photodiode array (PDA) detector was set at 210 nm. Experimental results showed that under the optimal conditions (column temperature, 40 ℃; and back pressure, 13.79 MPa), qualitative and quantitative analysis of the nine acrylates was completed within 4 min. Linear ranges were 0.2–100 mg/L for phenyl methacrylate (PNMA), benzyl methacrylate (BZMA) and ethylene dimethacrylate (EDMA); 0.3–100 mg/L for methacrylic acid (MAA); 0.4–100 mg/L for butyl acrylate (BTA), hydroxyethyl methylacrylate (HEMA) and hydroxyethyl acrylate (HEA); and 0.5–100 mg/L for isobutylmeth acrylate (IBMA) and benzyl acrylate (BZA). The determination coefficients (R2) of the standard curves for all acrylates were higher than 0.998 5, and recoveries obtained at high (30 mg/kg), middle (6 mg/kg) and low (0.2, 0.3, 0.4 and 0.5 mg/kg) spiked concentrations ranged from 89.3% to 109.7%, with relative standard deviations of 0.62% to 3.86% (n = 6). The limits of detection (RSN ≥ 3) were 0.05–0.15 mg/kg, and the limits of quantification (RSN ≥ 10) were 0.2–0.5 mg/kg. The proposed method identified the risk of acrylate residues in 30 batches of actual samples

COVID-19 Shock and the Time-Varying Volatility Spillovers Among the Energy and Precious Metals Markets: Evidence From A DCC-GARCH-CONNECTEDNESS Approach

The outbreak of the COVID-19 epidemic intensified the volatility of commodity markets (the energy and precious metals markets), which created a significant negative impact on the volatility spillovers among these markets. It may also have triggered a new volatility risk contagion. In this paper, we introduce the DCC-GARCH-CONNECTEDNESS approach to explore the volatility spillover level and multi-level spillover structure characteristics among the commodity markets before and during the COVID-19 epidemic in order to clarify the new volatility risk contagion patterns across the markets. The results implied several conclusions. (i) The COVID-19 epidemic has significantly improved the total volatility spillover level of the energy and precious metals markets and has enhanced the risk connectivity among the markets. (ii) The COVID-19 epidemic has amplified the volatility of the crude oil market, making it the main volatility spillover market, namely the source of volatility risk contagion. (iii) The COVID-19 epidemic outbreak enhanced the external risk absorption capacity of the natural gas and silver markets, and the absorption level of the external volatility spillover improved significantly. Furthermore, the risk absorption capacity of the gold market weakened, while the gold market has remained the endpoint of external volatility risk during the epidemic and has acted as a risk stabilizer. (iv) The volatility spillover among markets has clear time-varying characteristics and a positive connectedness with the severity of the COVID-19 epidemic. As the severity of the COVID-19 epidemic increases, the volatility risk connectivity among the markets rapidly increases