Monometallic Pt catalysts supported on mesoporous (MP) ZrO 2 were prepared and utilized as catalysts in the aqueous-phase upgrading of lignocellulosic biomass-derived levulinic acid (LA), with formic acid (FA) serving as a sustainable reducing agent. Among the studied catalysts, 1.6Pt/mesoporous ZrO 2 showed the highest LA conversion (97%) and a γ-valerolactone (GVL) yield (90%) at 513 K after 24 h of reaction was achieved. This high LA conversion and GVL yield obtained can be attributed to the high specific surface area (204 m 2 g −1 ) and density of acid sites (136 μmol g −1 ) and Pt dispersion (37%). Furthermore, this catalyst exhibits high stability after 96 h of reaction time, that is, four catalytic repetitions, with a GVL yield above 60% and no change in the crystal structure of the support. A high reaction temperature (533 K) tends to shift the reaction equilibrium from GVL to pentanoic acid which is formed with a yield of 22% after 24 h. Even after increasing the complexity of the model mixture by adding vanillin (V) as a lignin-derived model compound to the aqueous solution of LA and FA, the catalyst remained stable and the hydrogenation of LA and V succeeded, resulting in 43% of GVL and 65% of 2-methoxy-4-methylphenol after 24 h at 513 K.
The epoxidation of the unsaturated fatty acid methyl esters (FAME) in biodiesel with H2O2 was investigated at 323 K in the liquid phase over microporous nano-sized TS-1 as well as micro-/mesoporous nano-sized TS-1.
Peroxisome proliferator-activated receptor (PPAR)-gamma ligands are insulin sensitizers, widely used in the treatment of type 2 diabetes. A consistent observation in preclinical species is the development of cardiac hypertrophy after short-term treatment with these agents. The mechanisms for this hypertrophy are incompletely understood. Given the important role of insulin signaling in the regulation of myocardial size, we tested the hypothesis that augmentation of myocardial insulin signaling may play a role in PPAR-gamma ligand-induced cardiac hypertrophy. We treated mice with cardiomyocyte-restricted knockout of insulin receptors (CIRKO) and littermate controls (wild type) with 2-(2-(4-phenoxy-2-propylphenoxy) ethyl) indole-5-acetic acid (COOH), which is a non-thiazolidinedione PPAR-gamma agonist for 2 wk. Two weeks of COOH treatment increased heart weights by 22% in CIRKO mice and 16% in wild type, and induced similar fold increase in the expression of hypertrophic markers such as alpha-skeletal actin, brain natriuretic peptide, and atrial natriuretic peptide in CIRKO and wild-type (WT) hearts. COOH treatment increased plasma volume by 10% in COOH-treated WT and CIRKO mice but did not increase systolic or diastolic blood pressure. Echocardiographic analysis was also consistent with volume overload, as evidenced by increased left ventricular diastolic diameters and cardiac output in COOH-treated CIRKO and WT mice. These data indicate that cardiac hypertrophy after PPAR-gamma agonist treatment can occur in the absence of myocardial insulin signaling and is likely secondary to the hemodynamic consequences of plasma volume expansion.
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