Pathways for H₂ Activation on (Ni)-MoS₂ Catalysts

The activation of H₂ and H₂S on (Ni)­MoS₂/Al₂O₃ 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 H₂ and H₂S adsorption shows that both molecules dissociate on coordinatively unsaturated cations and neighboring S^2–. In the studied materials, one sulfur vacancy and four SH groups per 10 metal atoms exist at the active edges of MoS₂ under the conditions studied. H₂–D₂ 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 H₂ and H₂S chemisorption sites

The picture of leukocyte infiltration of the lung tissue of I/St (left) and B6 (right) mice infected with 2×10³ 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 2×10³ CFU of <i>M. avium</i> via aerosol route 8 weeks earlier.

<p>Peroxidase immune staining with hematoxylin counter-staining (×150). 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 Hypoxyprobe™-1 and sacrificed 3 h later. Lung cryosections were obtained and developed for indirect peroxidase staining to detect hypoxia gradients (×200).</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 [³H]-uracil uptake at 72 h after establishing co-cultures. 1 µCi/well [³H]-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 ± 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)  =  I/St; (B)  =  B6. Hypoxiprobe peroxidase staining (×25).</p

Effects of the Support on the Performance and Promotion of (Ni)MoS₂ Catalysts for Simultaneous Hydrodenitrogenation and Hydrodesulfurization

MoS₂ and Ni-promoted MoS₂ catalysts supported on γ-Al₂O₃, 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 MoS₂ 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 MoS₂ catalysts, HDS was strongly inhibited by NH₃, 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 Ni–Mo–S phase. Furthermore, the acidity of the support influences the acidity of the supported sulfide phase, which may play an important role in HDN