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This communication describes the synthesis of Pt@CeO2 core-shell catalysts for the application of highly efficient CO oxidation, where the 50% CO conversion temperature is lower than 200 °C. Pt@CeO2 is thermally stable as no deactivation occurs during the 70 h reaction, and the morphology is unchanged even after 700 °C thermal treatment.

This communication describes the design and synthesis of anti-sintering and -coke nickel phyllosilicate (PS) nanotubes (Ni/PSn) for hydrogen production via reforming reactions. The introduction of nickel particles in PS nanotubes could effectively maintain the Ni size and increase the resistance of metal particles for carbon deposition.

This communication describes the synthesis of a nanocomposite Ni@ZrO2 catalyst with enhanced metal-support interaction by introducing metal nanoparticles into the framework of the oxide support. The catalyst shows high catalytic activity and stability for hydrogen production via steam reforming of ethanol.

Background: This study was designed to investigate the effects of treatment with autologous mesenchymal stem cells (MSCs) by intracoronary transplantation on myocardial infarction (MI) in swine., Methods: MSCs were transfected with a lentiviral vector carrying the gene encoding green fluorescent protein (GFP) and labeled in vitro with superparamagnetic iron oxide (SPIO). An acute MI (AMI) model was established by percutaneous balloon occlusion. Dual-labeled MSC suspensions were injected through the infarct-related coronary artery using an over-the-wire (OTW) balloon device in the experimental group (n=5), while normal saline was injected into the control (n=5). Stem cell migration and improvements of cardiac function were evaluated by magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), and ultrasonic cardiogram (UCG) both before MSC transplantation and after 8 weeks. At 8weeks after transplantation, myocardial tissue was analyzed by histopathologic analyses., Results: Blue SPIO particles were in the cytoplasm of the MSCs. The labeling efficiency reached 100%. MRI revealed hypointensities of SPIO-labeled MSCs that were clustered in the myocardial infarct area after MSC transplantation. As time progressed, the signal gradually weakened and the area shrank. SPECT revealed that the myocardial filling defect was reduced and the amount of surviving myocardium was significantly increased at 8weeks. UCG revealed significant improvement when compared with the control at 8 weeks after transplantation. Prussian blue-positive cells were observed in the MI border zone. Fluorescence-positive cells were also observed, but the number of such cells was fewer than before., Conclusions: In vivo serial tracking of SPIO-labeled MSCs can be achieved by MRI. Intracoronary transplantation of SPIO-labeled MSCs can increase cardiac function and promote myocardial viability., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Although the role of the ubiquitin-proteasome system (UPS) in cardiac hypertrophy induced by pressure overload has been consistently studied, the fundamental importance of the UPS in cardiac fibrosis has received much less attention. Our previous study found that proteasome inhibitor (MG132) treatment attenuated cardiac fibrosis and heart failure during the early and middle stages of pressure overload. However, the effects of this inhibitor on late-stage pressure overload hearts remain unclear and controversial. The present study was designed to investigate the effects and possible mechanisms of MG132 on cardiac fibrosis and dysfunction during the late stages of pressure overload. Male Sprague Dawley rats with abdominal aortic constriction (AAC) or a sham operation received an intraperitoneal injection of MG132 (0.1 mg kg⁻¹ day⁻¹) or vehicle for 16 weeks. Left ventricular (LV) function, collagen deposition and Ang II levels were evaluated at study termination. Ang II-stimulated adult rat cardiac fibroblasts were utilized to examine the effects of MG132 on collagen synthesis and the relationship between the renin-angiotensin-aldosterone system (RAAS) and the UPS. MG132 treatment attenuated ventricular dysfunction by suppressing cardiac fibrosis rather than inhibiting cardiac hypertrophy during the late-stages of pressure overload. We also found that Ang II activates UPS in the heart and MG132 attenuates Ang II-induced collagen synthesis via suppression of the NF-κB/TGF-β/Smad2 signaling pathways. Proteasome inhibition therefore could provide a new promising therapeutic strategy to prevent cardiac fibrosis and progression of heart failure even during the late-stages of pressure overload., (Copyright © 2012 Elsevier Inc. All rights reserved.)

This paper describes a strategy for producing hydrogen via steam reforming of ethylene glycol over supported nickel catalysts. Nickel plays a crucial role in conversion of ethylene glycol and production of hydrogen, while oxide supports affect product distribution of carbonaceous species. A plausible reaction pathway is proposed based on our results and the literature.

This paper describes the utilization of skeletal Ni-based catalysts for steam reforming of ethanol to produce CO-free hydrogen, which could be superior in the application of fuel cells. Assistant metals play different roles in the reaction; Pt and Cu suppress the methanation and enhance H(2) production, while Co promotes the methanation.

Introduction: Our objective was to trace and evaluate intracoronary transplanted mesenchymal stem cells (MSCs) labelled with superparamagnetic iron oxide (SPIO) by using magnetic resonance imaging (MRI) in a swine model of myocardial infarction (MI)., Methods: MSCs were transfected with a lentiviral vector carrying the gene encoding green fluorescent protein (GFP) and labelled in vitro with SPIO. At 2 weeks after MI, swine were randomized to intracoronary transplantation of dual-labelled MSCs (n=10), MSC-GFP (n=10), and saline (n=5). MRI examination was performed with a 1.5-T clinical scanner at 24 hours, 3 weeks, and 8 weeks after cell transplantation. Signal intensity changes, cardiac function, and MI size were measured by means of MRI. The correlation between MRI findings and histomorphologic findings was also investigated., Results: MSCs could be efficiently and safely labelled with SPIO and GFP, and multipotentiality was not affected, especially for cardiomyocyte-like cell differentiation. Signal intensity on T2*-weighted imaging decreased substantially in the interventricular septum 24 hours after injection of MSCs. The intensity of hypointense signals appeared to increase throughout the later time points. Both dual-labelled MSCs and MSC-GFP could dramatically reduce the size of MI and improve cardiac function. Histologic data revealed that cells positive for Prussian blue stain were found mainly in the border zone, which also showed green fluorescence., Conclusions: In vivo 8-week tracing of dual-labelled MSCs can be achieved by MRI. Intracoronary transplantation of dual-labelled MSCs can increase cardiac function and reduce the size of MI in a swine model., (Copyright © 2011 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Estrogen promotes breast cancer metastasis. However, the detailed mechanism remains largely unknown. The actin binding protein ezrin is a key component in tumor metastasis and its over-expression is positively correlated to the poor outcome of breast cancer. In this study, we investigate the effects of 17β-estradiol (E2) on the activation of ezrin and its role in estrogen-dependent breast cancer cell movement. In T47-D breast cancer cells, E2 rapidly enhances ezrin phosphorylation at Thr(567) in a time- and concentration-dependent manner. The signalling cascade implicated in this action involves estrogen receptor (ER) interaction with the non-receptor tyrosine kinase c-Src, which activates the phosphatidylinositol-3 kinase/Akt pathway and the small GTPase RhoA/Rho-associated kinase (ROCK-2) complex. E2 enhances the horizontal cell migration and invasion of T47-D breast cancer cells in three-dimensional matrices, which is reversed by transfection of cells with specific ezrin siRNAs. In conclusion, E2 promotes breast cancer cell movement and invasion by the activation of ezrin. These results provide novel insights into the effects of estrogen on breast cancer progression and highlight potential targets to treat endocrine-sensitive breast cancers.

The nuclear factor (NF)-κB signaling pathway is an important intracellular mediator of cardiac hypertrophy. Recent studies have indicated that the anti-malarial agent artemisinin has the ability to inhibit NF-κB activation. We hypothesized that artemisinin would suppress cardiac hypertrophy by inhibiting NF-κB signal pathways. We tested this hypothesis using primary cultured rat cardiac myocytes and well-established rat models of cardiac hypertrophy. Artemisinin blocked angiotensin II-induced cardiac hypertrophy in vitro in a concentration-dependent manner. Furthermore, artemisinin protected against rat cardiac hypertrophy induced by transaortic constriction (TAC), as assessed by heart weight/body weight and lung weight/body weight ratios, echocardiographic parameters, and gene expression of hypertrophic markers. Electrophoretic mobility shift assays revealed increased NF-κB binding activity in cardiac nuclear extracts of banded rats that was prevented by artemisinin treatment. Banded rats treated with oral artemisinin, compared with untreated rats, showed significantly decreased the levels of IL-6, TNF-α and MCP-1 mRNA expression and increased protein levels of IκB-α, which forms a cytoplasmic inactive complex with the p65-p50 heterodimeric complex. The effect of artemisinin on cardiac hypertrophy was blocked after IκB-α was silenced by transfection of cardiomyocytes with IκB-α siRNA. Our results indicate that artemisinin inhibits cardiomyocyte growth by interfering with NF-κB signaling., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Proteasome inhibitors are involved in cell cycle control, growth and inflammatory signaling, and transcriptional regulation of mitotic cells. A recent study has suggested that specific proteasome inhibitor MG132 may suppress cardiomyocyte hypertrophy in vitro. However, the underlying molecular mechanisms are not clear. In this study, we investigated the effects of long-term MG132 treatment on cardiac hypertrophy and the related molecular mechanisms in vivo. MG132 (0.1 mg/kg/day) was intraperitoneally injected to rats with abdominal aortic banding (AAB) for 8 weeks. Results showed that treatment with MG132 significantly attenuated left ventricular (LV) myocyte area, LV weight/body weight, and lung weight/body weight ratios, decreased LV diastolic diameter and wall thickness, and increased fractional shortening in AAB rats. AAB induced the phosphorylation of ERK1/2, JNK1, and p38 in cardiac myocytes. The elevated phosphorylation levels of ERK1/2 and JNK1 in AAB rats were significantly reversed by MG132 treatment. In conclusion, our results suggested that long-term treatment with MG132 attenuates pressureoverload-induced cardiac hypertrophy and improves cardiac function in AAB rats through regulation of ERK1/2 and JNK1 signaling pathways.

Objective: Vascular endothelial growth factor (VEGF), angiopoietin (Ang)-1 and -2 regulate angiogenesis and might be important in myocardial collateral development. Elevated levels of angiogenic growth factors in patients with coronary artery disease (CAD) have been reported. However, the age-related change of angiogenic growth factors in patients with CAD remains unclear., Methods and Results: Serum VEGF, Ang-1 and -2 levels were measured by enzyme-linked immunosorbent assay kits. Serum VEGF, Ang-1 and -2 levels in patients with CAD were significantly higher than those in healthy control subjects. In patients aged <61 years and 61 to 70 years, serum Ang-1 and -2 levels were significantly higher than in patients aged >70 years, serum Ang-2 levels in patients aged <61 years were significantly higher than in patients aged from 61 to 70 years. Serum VEGF levels were not significantly different in the three age groups. Serum VEGF, Ang-1 and -2 levels were not significantly different across the age groups in healthy subjects. Regression analysis showed that there was a negative correlation between age and Ang-1 and -2 in patients with CAD., Conclusion: Serum Ang-1 and -2 levels, but notVEGF levels in patients with CAD, are decreased along with advancing age.

Although short-term B-type natriuretic peptide (BNP) treatment has been shown to be effective for decompensated congestive heart failure, little is known about the effects of long-term BNP treatment in ventricular remodeling and heart failure in response to myocardial infarction. The aim of the present study was to investigate the effects of long-term BNP treatment on ventricular remodeling and heart failure after myocardial infarction in rats. Myocardial infarction was induced by ligating the left anterior descending coronary artery. The surviving rats were randomly divided into four groups: 1) vehicle-treated myocardial infarction group ('vehicle-treated group'), 2) rats treated with low-dose BNP ('low BNP group'), 3) rats treated with high-dose BNP ('high BNP group'), 4) sham-operated group. Eight weeks after the operation, rats were sacrificed. Compared with the sham-operated group, the vehicle-treated group had significantly higher collagen deposition and angiotensin II levels (P<0.01) and a significantly lower cardiac function (P<0.05). Both BNP-treated groups had significant improvement of these indexes compared with the vehicle-treated group (P<0.01). The high BNP group had significantly less collagen deposition and better cardiac function than the untreated and low BNP groups. Moreover, the mRNA and protein expression of TGFbeta1 and Smad2 in the vehicle-treated group was significantly higher than in the sham-operated group (P<0.01). Both BNP-treated groups had a suppression of TGFbeta1 and Smad2 expression (P<0.01). In conclusion, long-term treatment with BNP prevents ventricular remodeling and deterioration of cardiac function in a dose-dependent fashion, a process that may be associated with the inhibition of TGFbeta1/ Smad2 signaling.

1. It is reported that alpha1-receptors and adenosine A1-receptors are involved in the ischaemic preconditioning (PC) effect on infarct size (IS). However, it is still unclear to what extent alpha1-receptors and adenosine A1-receptors contribute to the mechanism of PC. Therefore, we investigated the extent of the contribution of alpha1-receptors and adenosine A1 receptors to the PC effect on IS and examined the relationship between these receptors and protein kinase C. 2. Infarct size was measured in rabbits subjected to 30 min ischaemia and 48 h reperfusion. Tyramine (Tyr) was intravenously administered before 30 min ischaemia in the absence or presence of bunazosin (BN, alpha1-receptor blocker) and staurosporine (ST), a protein kinase C inhibitor, respectively. R(-)N6-(2-phenylisapropyl)-adenosine (PIA), a selective adenosine A1 agonist, was intravenously administered before 30 min ischaemia in the absence or presence of 8-p-sulphophenyltheophylline (8SPT), an adenosine blocker and ST, respectively. In the PC groups, BN, BN + PIA, 8SPT, 8SPT + Tyr or placebo saline was injected before or during PC. 3. Both Tyr and PIA reduced the IS, which was blocked by BN and 8SPT, respectively. The IS-reducing effect of Tyr or PIA was blocked by ST. The IS-reducing effect of PC was completely blocked by BN and 8SPT, respectively. The blocking effect of BN on the IS-reducing effect of PC was abolished by adding PIA during PC ischaemia. The blocking effect of 8SPT on the IS-reducing effect of PC was abolished by adding Tyr before PC ischaemia. 4. These data suggest that an alpha1-receptor dependent pathway exists and an adenosine A1-receptor dependent pathway, stimulation of both of which activates protein kinase C, then reduces the IS. However, exclusive stimulation of a single alpha1-receptor dependent pathway or a single adenosine A1-receptor dependent pathway alone is not sufficient but the summation of these pathways is required to achieve a PC effect on IS in rabbits.