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To improve the capacity for complete oxidation of gaseous benzene by catalytic ozonation, a series of metal oxides catalysts (Mn, Co, Ni, Cu, Zn and Ce) were prepared by impregnation method using ZSM-5 zeolite as the support. The developed metal oxides were highly dispersed in nanosize on the support. Among them, MnO2/ZSM-5 showed the best activity toward catalytic ozonation of benzene. Benzene can be completely removed even at room temperature and CO2 selectivity reached 84.7%. MnO2/ZSM-5 was quite effective due to the production of highly reactive oxidizing species from ozone decomposition. The activities toward benzene catalytic ozonation are closely related to the capacity for ozone decomposition.

Highly dispersed MnO 2 nanoparticles were supported on ZSM-5 zeolite and used for ozone-catalytic oxidation (OZCO) of gaseous benzene. The prepared MnO 2 /ZSM-5 is very active in complete oxidation of benzene even at ambient temperature. Benzene conversion and CO 2 selectivity reached 100% and 84.7%, respectively, while no CO byproduct was formed. However, while it ran well in air with low humidity, the catalyst got slowly deactivated after a long run in humid air. The possible reasons responsible for its deactivation were investigated. The structural changes of catalysts and the intermediates generated from benzene oxidation should not be the key cause for catalytic deactivation. Benzene OZCO is highly sensitive to water vapor and water poisoning mainly accounted for the deactivation of MnO 2 /ZSM-5 due to its occupying of catalytic active sites and adsorption centers. The improved catalytic activity and suppression of deactivation can be easily achieved by reducing water vapor or slightly increasing reaction temperature.

The objective of the present study was to test the hypothesis that brain Na, K-ATPase expression and/or activity is altered following an increase in blood pressure produced by constriction of the abdominal aorta just proximal to the renal arteries. A suprarenal constriction (SRC) was made to conform to the diameter of a 19-gauge (19-G) or 20-gauge (20-G) needle, while in a sham-operated group (Sham) the aorta was exposed surgically but not constricted. Within 1 week of SRC, mean arterial pressure was increased and remained elevated at 4 weeks post surgery. At 1 week, whole-brain Na, K-ATPase mRNA levels were depressed for all isoforms (alpha1 approximately beta1alpha2alpha3). No changes were observed in the hypothalamus. At 4 weeks, the mRNA levels of all alpha isoforms were significantly increased in the whole brain and these changes were paralleled by an increase of alpha2 and alpha3 transcript in the hypothalamus. beta1 mRNA expression was increased in the hypothalamus only. The alpha-isoform protein expression generally changed in the same direction as mRNA changes at both 1 and 4 weeks, as did alpha1 enzyme activity at 1 week and the combined alpha2/alpha3 enzyme activities at 4 weeks. Since inhibition of brain Na, K-ATPase increases sympathetic nervous system (SNS) activity and blood pressure, the decreases in brain Na, K-ATPase expression and activity at 1 week post SRC may contribute to the hypertension during its developmental phase, while the increase in the alpha2/alpha3 brain expression and activity at 4 weeks may be a compensatory response to established hypertension.

Although captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been shown to exert a beneficial effect on cardiac function in heart failure, its effect on the status of sarcoplasmic reticulum (SR) Ca(2+) transport in the failing heart has not been examined previously. In order to determine whether captopril has a protective action on cardiac function, as well as cardiac SR Ca(2+)-pump activity and gene expression, a rat model of heart failure due to myocardial infarction was employed in this study. Sham operated and infarcted rats were given captopril (2 g/l) in drinking water; this treatment was started at either 3 or 21 days and was carried out until 8 weeks after the surgery. The untreated animals with myocardial infarction showed increased heart weight and elevated left ventricular end diastolic pressure, reduced rates of pressure development and pressure fall, as well as depressed SR Ca(2+) uptake and Ca(2+)-stimulated ATPase activities in comparison with the sham control group. These hemodynamic and biochemical changes in the failing hearts were prevented by treatment of the infarcted animals with captopril. Likewise, the observed reductions in the SR Ca(2+) pump and phospholamban protein contents, as well as in the mRNA levels for SR Ca(2+) pump ATPase and phospholamban, in the failing heart were attenuated by captopril treatment. These results suggest that heart failure is associated with a defect in the SR Ca(2+) handling and a depression in the gene expression of SR proteins; the beneficial effect of captopril in heart failure may be due to its ability to prevent remodeling of the cardiac SR membrane.