7 research outputs found
Pathways for H<sub>2</sub> Activation on (Ni)-MoS<sub>2</sub> Catalysts
The activation of H<sub>2</sub> and
H<sub>2</sub>S on (Ni)ĀMoS<sub>2</sub>/Al<sub>2</sub>O<sub>3</sub> leads
to the formation of SH
groups with acid character able to protonate 2,6-dimethylpyridine.
The variation in concentrations of SH groups induced by H<sub>2</sub> and H<sub>2</sub>S adsorption shows that both molecules dissociate
on coordinatively unsaturated cations and neighboring S<sup>2ā</sup>. In the studied materials, one sulfur vacancy and four SH groups
per 10 metal atoms exist at the active edges of MoS<sub>2</sub> under
the conditions studied. H<sub>2</sub>āD<sub>2</sub> exchange
studies show that Ni increases the concentration of active surface
hydrogen by up to 30% at the optimum Ni loading, by increasing the
concentration of H<sub>2</sub> and H<sub>2</sub>S chemisorption sites
The picture of leukocyte infiltration of the lung tissue of I/St (left) and B6 (right) mice infected with 2Ć10<sup>3</sup> CFU of <i>M. avium</i> via aerosol route 16 weeks earlier.
<p>See legend to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010515#pone-0010515-g002" target="_blank">Fig. 2</a>.</p
The picture of leukocyte infiltration of the lung tissue of I/St (left) and B6 (right) mice infected with 2Ć10<sup>3</sup> CFU of <i>M. avium</i> via aerosol route 8 weeks earlier.
<p>Peroxidase immune staining with hematoxylin counter-staining (Ć150). Cell populations are indicated on the left side. See text for the description.</p
The lung tissue surrounding necrotizing granuloma centers in mice susceptible to <i>M. tuberculosis</i> and <i>M. avium</i> is markedly hypoxic.
<p>I/St mice 6 wk after <i>M. tuberculosis</i> challenge (A) and B6 mice 16 wk after <i>M. avium</i> challenge (B) were injected with 60 mg/kg body weight of Hypoxyprobeā¢-1 and sacrificed 3 h later. Lung cryosections were obtained and developed for indirect peroxidase staining to detect hypoxia gradients (Ć200).</p
B6 mice are more resistant to <i>M. tuberculosis</i> infection compared to I/St mice.
<p>Their survival time (A, <i>P</i><0.001, Gohen's criterion for survival curves) is longer and lung CFU counts (B, <i>P</i><0.01-0.001 at different time points, ANOVA) are lower. Lung macrophages of I/St, but not of B6, mice inhibit multiplication of <i>M. avium</i> after in vitro infection within a high range of MOI (C). The rate of mycobacterial growth was measured by [<sup>3</sup>H]-uracil uptake at 72 h after establishing co-cultures. 1 ĀµCi/well [<sup>3</sup>H]-uracil was added for the last 18 h of incubation. The wells containing mycobacteria alone at numbers corresponding to each MOI served as controls. Results obtained in one of three similar experiments are expressed as mean CPMs Ā± SD for triplicate cultures; interstrain differences are statistically significant (<i>P</i><0.01, Mann-Whitney's U-test).</p
<i>M. avium</i> infection does not render active hypoxia in the lungs of resistant mice, but induces numerous necrotizing granuloma surrounded by hypoxic zones in the lungs of susceptible mice.
<p>(A) ā=ā I/St; (B) ā=ā B6. Hypoxiprobe peroxidase staining (Ć25).</p
Effects of the Support on the Performance and Promotion of (Ni)MoS<sub>2</sub> Catalysts for Simultaneous Hydrodenitrogenation and Hydrodesulfurization
MoS<sub>2</sub> and Ni-promoted MoS<sub>2</sub> catalysts supported
on Ī³-Al<sub>2</sub>O<sub>3</sub>, siliceous SBA-15, and Zr-
and Ti-modified SBA-15 were explored for the simultaneous hydrodesulfurization
(HDS) of dibenzothiophene (DBT) and hydrodenitrogenation (HDN) of <i>o</i>-propylaniline (OPA). In all cases, OPA reacted preferentially
via initial hydrogenation, and DBT was converted through direct sulfur
removal. HDN and HDS activities of MoS<sub>2</sub> catalysts are determined
by the dispersion of the sulfide phase. Ni promotion increased its
dispersion and activity for DBT HDS and also increased the rate of
HDN via enhancing the rate of hydrogenation. On nonpromoted MoS<sub>2</sub> catalysts, HDS was strongly inhibited by NH<sub>3</sub>,
and the addition of Ni dramatically reduced this inhibiting effect.
The conclusion is that HDS is proportional to the concentration of
Mo and Ni on the edges of sulfide particles. In contrast, the direct
hydrodenitrogenation of OPA occurs only on accessible Mo cations and,
hence, decreases with increasing Ni substitution. The nature of the
support influences the dispersion of the nonpromoted catalysts as
well as the decoration degree of Ni on the edges of the NiāMoāS
phase. Furthermore, the acidity of the support influences the acidity
of the supported sulfide phase, which may play an important role in
HDN