Catalytic behavior of NaV6O15 bronze for partial oxidation of hydrogen sulfide

[EN] Na-containing V2O5 materials have been prepared hydrothermally from gels with Na/V ratios of 0.02-0.26, and calcined at 500 degrees C. The calcined samples have been characterized and tested as catalysts in the partial oxidation of H2S to elemental sulfur. At low Na-contents, V2O5 and NaV6O15 bronze are formed, with the NaV6O15/V2O5 ratio increasing with the Na-content. Pure NaV6O15 bronze is mainly formed from gels containing a Na/V ratio of 0.18. However, NaV6O15 and Na1.164V3O8 are formed from gels with Na/V ratio higher than 0.35. NaV6O15 based catalyst shows high conversion for the oxidation of H2S with a high selectivity into elemental sulfur. These catalysts are more active and stable than pure or Na-doped V2O5 catalysts. V4O9 is observed after reaction in both pure Na-doped V2O5 catalysts but also in NaV6O15/V2O5 mixed catalysts. However, no changes in the NaV6O15 crystalline structure are observed in the Na-promoted catalysts. Accordingly, NaV6O15 crystalline phase is stable for several hours of catalysisat a difference with V2O5. The active sites in V-containing vanadium catalysts are probably V5+-O-V4+ pairs as previously proposed for V4O9 crystalline phase. The best catalytic performances were achieved on V2O5-NaV6O15 mixtures which are transformed into V4O9-NaV6O15 mixtures during the catalytic tests. These catalytic results could be due to the intrinsic physical properties of both phases but also because of the optimal dispersion obtained in the synthesis procedure. (C) 2014 Elsevier B.V. All rights reserved.The authors would like to thank the DGICYT in Spain (Projects CTQ2012-37925-C03-01, CTQ2012-37925-C03-03 and MAT2010-19837-C06-05) for financial support.Soriano Rodríguez, MD.; Rodriguez-Castellon, E.; Garcia-Gonzalez, E.; López Nieto, JM. (2014). Catalytic behavior of NaV6O15 bronze for partial oxidation of hydrogen sulfide. Catalysis Today. 238:62-68. https://doi.org/10.1016/j.cattod.2014.02.030S626823

Effects of glutamine and hyperoxia on pulmonary oxygen uptake and muscle deoxygenation kinetics.

The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max