The interaction of atomic hydrogen and H 2 O with stoichiometric and partially reduced CeO 2 (111) thin films deposited on a Cu(111) substrate was investigated by temperature programmed desorption and X-ray photoelectron spectroscopy. On stoichiometric CeO 2 (111) surface, the adsorption of atomic H(g) leads to the formation of surface hydroxyl (OH(a)) and H 2 O(a) as well as the reduction of Ce 4+ into Ce 3+ . On reduced CeO 2 (111) surfaces, the stability of OH(a) was enhanced by the presence of oxygen vacancies. Upon heating, surface hydroxyls undergo two competing reaction pathways: one is the associative desorption of OH(a) releasing H 2 O and creating oxygen vacancies (OH(a) + OH(a) → H 2 O(g) + O lattice + O vacancy ), and the other one is to produce H 2 via OH(a) + OH(a) → H 2 (g) + 2O lattice . The presence of oxygen vacancies in CeO 2 favors the reaction pathway of H 2 formation. At 115 K, reversible dissociation and molecular adsorption of H 2 O occur on stoichiometric CeO 2 (111) surface, but irreversible dissociation of H 2 O occurs on reduced CeO 2 (111) surfaces. These results deepen the fundamental understanding of the influence of oxygen vacancies on the reactivity of surface hydroxyls and water on CeO 2 surface.

Persistent airway inflammation, mucus production, and airway hyperreactivity are the major contributors to the frequency and severity of asthma. Why lung inflammation persists in asthmatics remains unclear. It has been proposed that Fas-mediated apoptosis of inflammatory cells is a fundamental mechanism involved in the resolution of eosinophilic airway inflammation. Because infiltrating eosinophils are highly sensitive to Fas-mediated apoptosis, it has been presumed that direct ligation of Fas on eosinophils is involved. Here, we utilize adoptive transfers of T cells to demonstrate that the delayed resolution of eosinophilia in Fas-deficient mice is a downstream effect of Fas deficiency on T cells, not eosinophils. Interestingly, the mice that received Fas-deficient T cells, but not the controls, developed a persistent phase of inflammation that failed to resolve even 6 wk after the last challenge. This persistent phase correlated with decreased interferon (IFN)γ production by Fas-deficient T cells and could be reproduced with adoptive transfer of IFNγ-deficient T cells. These data demonstrate that Fas deficiency on T cells is sufficient for the development of long-term allergic airway disease in mice and implies that deregulation of death receptors such as Fas on human T cells could be an important factor in the development and/or chronic nature of asthma.

We have investigated the adsorption of water on a Co(0001) surface by means of temperature-programmed desorption (TPD), X-ray photoelectron spectroscopy (XPS), and low-energy electron diffraction (LEED). At 130 K, the interaction between adsorbed water (H 2 O(a)) and Co(0001) is quite weak, and water adsorption forms an intact, nonwetting, and three-dimensional layer on Co(0001). The monolayer and multilayer of H 2 O(a) could be distinguished by XPS, and they desorb molecularly upon heating but only giving a single water desorption peak. An ordered p(2 × 2) LEED pattern was observed at low exposures of water. At room temperature, water adsorbs dissociatively on Co(0001), forming chemisorbed atomic oxygen (O(a)) and atomic hydrogen (H(a)). Upon heating, H(a) recombines into H 2 desorbing from the surface, whereas O(a) remains on the surface. The interaction of water with Co( 0001) is greatly influenced by the presence and nature of the oxygen species on Co(0001). Water adsorption on Co(0001) precovered with 0.45 ML O(a) at 130 K forms a mixture layer of OH(a) and H(a) via the reaction of 2H 2 O(a) + O(a) f 3OH(a) + H(a). However, on oxide-like Co(0001) surface, the water decomposition is completely passivated even at room temperature. These results broaden our fundamental understanding of water interaction with metal surfaces and provide insights into the water-involved catalytic reactions catalyzed by cobalt. † Part of the "D. Wayne Goodman Festschrift".