The mechanism responsible for the irreversible deactivation of ceria-supported precious metals for the watergas-shift reaction has been investigated through accelerated aging tests. It is shown that deactivation of Pd/ ceria occurs more rapidly at 673 K compared to 523 K when operating with an integral reactor in 25 torr each of CO and H 2 O. By heating a fresh catalyst in H 2 , H 2 O, CO, or CO 2 , it was shown that deactivation occurs due to the presence of CO. Measurements of metal dispersion by CO adsorption and by x-ray diffraction show that deactivation on Pt/ceria and Pd/ceria catalysts in our studies was due to a loss of metal surface area. Finally, water-gas-shift rates on a series Pd/ceria catalysts with ceria crystallite sizes ranging from 7.2 to 40 nm and Pd loadings of either 1 wt% or 6 wt% demonstrated that rates were strictly proportional to the Pd surface area. Based on these observations, ceria-supported precious metals could be active and stable for the watergas-shift reaction if steps are taken to avoid metal particle-size growth. AbstractThe mechanism responsible for the irreversible deactivation of ceria-supported precious metals for the water-gas-shift reaction has been investigated through accelerated aging tests. It is shown that deactivation of Pd/ceria occurs more rapidly at 673 K compared to 523 K when operating with an integral reactor in 25 torr each of CO and H 2 O. By heating a fresh catalyst in H 2 , H 2 O, CO, or CO 2 , it was shown that deactivation occurs due to the presence of CO.Measurements of metal dispersion by CO adsorption and by x-ray diffraction show that deactivation on Pt/ceria and Pd/ceria catalysts in our studies was due to a loss of metal surface area. Finally, water-gas-shift rates on a series Pd/ceria catalysts with ceria crystallite sizes ranging from 7.2 to 40 nm and Pd loadings of either 1 wt% or 6 wt% demonstrated that rates were strictly proportional to the Pd surface area. Based on these observations, ceria-supported precious metals could be active and stable for the water-gas-shift reaction if steps are taken to avoid metal particle-size growth.

The substance P (SP)-preferring receptor neurokinin-1 receptor (NK-1R) has two forms: a full-length receptor consisting of 407 aa and a truncated receptor consisting of 311 aa. These two receptors differ in the length of the C terminus of NK-1R. We studied the undifferentiated and phorbol myristate acetate (

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Sulfur–carbon composites were prepared by an in situ sulfur deposition route developed for the heterogeneous nucleation of sulfur into nanopores of conductive carbon black (CCB) by fumigation of Na2S4/CCB powder with HCl. The sulfur–carbon composites demonstrate enhanced reversible capacity and stable cycle performance.

We examined the gene expression and regulation of Type III interferon (IFN), IFN-λ, in human neuronal cells. Human neuronal cells expressed endogenous IFN-λ1 but not IFN-λ2/3. Upon the activation of Toll-like receptor (TLR)-3 expressed in the neuronal cells by polyriboinosinic polyribocytidylic acid (PolyI:C), both IFN-λ1 and IFN-λ2/3 expression was significantly induced. The activation of TLR-3 also exhibited antiviral activity against pseudotyped HIV-1 infection of the neuronal cells. Human neuronal cells also expressed functional IFN-λ receptor complex, interleukin-28 receptor α subunit (IL-28Rα) and IL-10Rβ, as evidenced by the observations that exogenous IFN-λ treatment inhibited pseudotyped HIV-1 infection of the neuronal cells and induced the expression of APOBEC3G/3F, the newly identified anti-HIV-1 cellular factors. These data provide direct and compelling evidence that there is intracellular expression and regulation of IFN-λ in human neuronal cells, which may have an important role in the innate neuronal protection against viral infections in the CNS. KeywordsInterferon (IFN); Toll-like receptor (TLR); NT2-N; Neuron; Virus; HIV Interferon lambda (IFN-λ), the newly discovered type III family of IFNs (Kotenko et al., 2003, Sheppard et al., 2003, comprises three structurally related cytokines, IFN-λ1, IFN-λ2 and IFN-λ3. A gene array experiment covering the whole human genome revealed that all the IFN-λinduced genes could also be activated by type I IFNs (Zhou et al., 2007). In addition,

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