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The reaction pathways leading to aromatic hydrocarbons such as benzene and naphthalene in gas-phase reactions of multi-component mixtures derived from cellulose fast pyrolysis were studied both experimentally and numerically. A two-stage tubular reactor was used for evaluating the reaction kinetics of secondary vapor phase cracking of the nascent pyrolysates at temperature ranging from 400 to 900 °C, residence time from 0.2 to 4.3 s, and at 241 kPa. The products of alkyne and diene were identified from the primary pyrolysis of cellulose even at low temperature range 500–600 °C. These products include acetylene, propyne, propadiene, vinylacetylene, and cyclopentadiene. Experiments were also numerically validated by a detailed chemical kinetic model consisting of more than 8000 elementary step-like reactions with over 500 chemical species. Acceptable capabilities of the kinetic model in predicting concentration profiles of the products enabled us to assess reaction pathways leading to benzene and naphthalene via the alkyne and diene from primary pyrolysates of cellulose. C3 alkyne and diene are primary precursors of benzene at 650 °C, while combination of ethylene and vinylacetylene produces benzene dominantly at 850 °C. Cyclopentadiene is a prominent precursor of naphthalene. Combination of acetylene with propyne or allyl radical leads to the formation of cyclopentadiene. Furan and acrolein are likely important alkyne precursors in cellulose pyrolysis at low temperature, whereas dehydrogenations of olefins are major route to alkyne at high temperatures.

This paper proposes catalytic hydrothermal reforming (CHTR) for producing substitute natural gas (SNG) directly from a lignin in aqueous alkaline media, which can fully dissolve the lignin but stabilize it, lowering the reactivity toward water. Among catalysts preliminarily tested, activated-carbon-supported ruthenium (Ru/AC) catalysts showed the highest activity in terms of reduction of the total organic carbon concentration (TOC) in the aqueous solution. CHTR of a lignin was performed employing a 5000 ppm TOC solution of 0.1 M Na2CO3 in a continuous reactor. The presence of Na2CO3 in the solution enabled delivery of the lignin, which is poorly soluble in water, to the reactor as well as suppression of char formation during CHTR. A Ru/AC showed its ability to maintain 98.6% conversion of the lignin at 350 °C even under the alkaline environment for a duration of at least 10 h, with colorless effluent liquid containing 70 ppm TOC of organic carbon. A low content of Ru in the Ru/AC resulted in an insufficie...

Oxidized LDL (oxLDL) has been shown to activate the sphingomyelinase pathway producing ceramide in vascular smooth muscle cells. Therefore ceramide, which is a biologically active lipid causing apoptosis in a variety of cells, may be involved in the apoptotic action of oxLDL. In this study, we examined whether cholesterol enriched diets affected ceramide metabolism and oxidation product of LDL, represented by degradation of apolipoprotein B-100 (apoB) in apoE-deficient (apoE-/-) mice. ApoE-/- and wild type mice were fed a standard (AIN-76) diet or 1% cholesterol-enriched diet for 8 weeks. Tissue ceramide levels were analyzed using electrospray tandem mass spectrometry (LC-MS/MS). Ceramide levels in the plasma and the liver of apoE-/- mice were intrinsically higher than those of the wild type. In apoE-/- mice, dietary cholesterol significantly increased several ceramides and degradation products of apoB in plasma compared to those fed the control diet. Dietary cholesterol did not affect tissue ceramide levels in the wild type mice. Based on these results, plasma ceramides possibly correlate with the increase in LDL oxidation and are a risk factor for atherosclerosis.

First principles, density functional theory embodied in the DMol program has been applied to agostic ethyl-Ti-complexes, including the dmpe complex, [Ti(-CH 2 CH 3 )C1 3 (dmpe)], where dmpe=(Me 2 PCH 2 ) 2 and its model complex, [Ti(−CH 2 CH 3 )Cl 3 (PH 3 ) 2 ]. The ethyl moiety of the complexes can adopt two limiting conformations, staggered and eclipsed. In the model complex, [Ti(−CH 2 CH 3 )C1 3 (PH 3 ) 2 ], both conformers are found to form agostic structures upon geometry optimization subject to Cs symmetry constraint, with the agostic eclipsed structure being the lower in energy. Full geometry optimization of the dmpe complex, [Ti(−CH 2 CH 3 )C1 3 (dmpe)], yields an agostic structure with geometrical features similar to those measured by single crystal X-ray analysis. It is shown that the HOMO orbital contributes substantially to the agostic bonding.

To study the effects of hexavalent and trivalent chromium on lipid peroxidation, isolated rat hepatocytes were incubated with different concentrations of chromium compounds at 37°C for 60min. Lipid peroxidation was determined as thiobarbituric acid (TBA)-reacting materials. Cellular injury was observed as a leakage of lactate dehydrogenase (LDH) from hepatocytes into incubation medium. The contents of reduced glutathione(GSH) in hepatocytes were also assessed. Results obtained were as follows: (1) Lipid peroxidation of isolated rat hepatocytes which was expressed as TBA-reactant formation was inhibited by trivalent chromium at the range of concentrations tested in this experiment (125∼1000μM). Hexavalent one inhibited lipid peroxidation at low concentration (125μM), but facilitated that at high concentration (1000μM). (2) LDH-leakage was facilitated by the addition of hexavalent chromium (K2Cr2O7, 125∼1000μM), on the other hand trivalent one (Cr(NO3)3) inhibited it significantly at concentrations more than 250μM. (3) The hexavalent chromium-induced lipid peroxidation was inhibited by antioxidants such as N, N'-dipheyl-p-phenylenediamine (DPPD), α-tocopherol and diethyl dithiocarbamate (DDTC). However, LDH-leakage from hepatocytes was not inhibited by these antioxidants. (4) After the pretreatment with GSH depleting agent such as diethyl maleate (DEM) on isolated hepatocytes, the lipid peroxidation induced by hexavalent chromium was significantly enhanced and was dependent on the chromium concentrations in the incubation medium. Furthermore this enhancement of lipid peroxidation was canceled by the addition of GSH (10mM). (5) The lipid peroxidation induced by ascorbate was significantly inhibited by the addition of hexavalent chromium as well as trivalent one. This effect of hexavalent chromium might be essentially due to the reduction of hexavalent chromium to trivalent one by ascorbate. These results suggest that chromium in trivalent form inhibits lipid peroxidation in isolated hepatocytes, while hexavalent one facilitates it but is not necessarily correlated to cellular injury.