Ionization of Rydberg H2 molecules at doped silicon surfaces.

The present study focuses on the interaction of H2 Rydberg molecules with doped silicon semiconductor surfaces. Para-H2 Rydberg states with principal quantum numbers n = 17-21 and core rotational quantum number N(+) = 2 are populated via resonant two-colour two-photon (vacuum ultraviolet-ultraviolet) excitation and collide at grazing incidence with a surface. For small Rydberg-surface separation, the Rydberg states are ionized due to the attractive surface potential experienced by the Rydberg electron and the remaining ion-core is detectable by applying a sufficiently strong external electric field. It is found that the surface ionization profiles (ion signal vs applied field) of H2 on p-type doped Si surfaces show a higher detected ion signal than for n-type Si surfaces, while an Au surface shows lower detected ion signal than either type of Si surface. It is shown that ion detectability decreases with increasing dopant density for both types of Si surfaces. Higher-n Rydberg states show higher ion detectability than lower-n Rydberg states but this variation becomes smaller when increasing the dopant density for both p- and n-type surfaces. Theoretical trajectory simulations were developed with a 2D surface potential model and using the over-the-barrier model for the ionization distance; the results help to explain the observed variations of the experimental surface ionization profiles with dopant density and type.

Level crossings in the ionization of H(2) Rydberg molecules at a metal surface.

The ionization of H(2) Rydberg states at a metal surface is investigated using a molecular beam incident at grazing incidence on a gold surface. The H(2) molecules, excited by stepwise two-color laser excitation, are selected in each of the accessible Stark eigenstates of the N(+) = 2, n = 17 Rydberg manifold in turn and the ionization at the surface is characterized by applying a field to extract the ions formed. Profiles of extracted ion signal versus applied field show resonances that can be simulated by assuming an enhancement of surface ionization at fields corresponding to energy-level crossings between the populated N(+) = 2 manifold and the near-degenerate N(+) = 0 Stark manifolds. It is concluded that the slow (microsecond time scale) rotation-electronic energy transfer to N(+) = 0 states occurring at these crossings takes place in the time interval following application of the field ramp when the molecule is still distant from, and unperturbed by, the surface. However, the energy levels are strongly perturbed by image-dipole interactions as the molecule approaches close to the surface, leading to additional energy-level crossings. Adiabatic behavior at such crossings affects the intensity of the observed resonances in the surface ionization signal but not their field positions. Resonances are also observed in the surface ionization profiles at fields above the field-ionization threshold; some of these show asymmetric "Fano-type" line shapes due to quantum interference in the nonradiative coupling to degenerate bound and continuum states.

Reactions of nitric oxide on Rh6+ clusters: abundant chemistry and evidence of structural isomers.

We report the first results of a new instrument for the study of the reactions of naked metal cluster ions using techniques developed by Professor Bondybey to whom this issue is dedicated. Rh6+ ions have been produced using a laser vaporization source and injected into a 3 T Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometer where they are exposed to a low pressure (< 10(-8) mbar) of nitric oxide, NO. This system exhibits abundant chemistry, the first stages of which we interpret as involving the dissociative chemisorption of multiple NO molecules, followed by the liberation of molecular nitrogen. This yields key intermediates such as [Rh6O2]+ and [Rh6O4]+. The formation of the latter, after adsorption of four NO molecules, marks a change in the chemistry observed with further NO molecules adsorbed (presumably molecularly) without further N2 evolution until saturation is apparently reached with the [Rh6O4(NO)7]+ species. We analyse the data in terms of a simple 12-stage reaction mechanism, and we report the relative rate constants for each step. The trends in reactivity are assessed in terms of conceivable structures and the results are discussed where appropriate by comparison with extended surface studies of the same system. Particular attention is paid to the first step in the reaction (Rh6(+) + NO --> [Rh6NO]+) which exhibits distinctly bi-exponential kinetics, an observation we interpret as evidence for two different structural isomers of the Rh6+ cluster with one reacting more than an order of magnitude faster than the other.

Infusion of in vitro-generated DN T regulatory cells induces permanent cardiac allograft survival in mice.

Previously, we have demonstrated that pretransplant donor lymphocyte infusion (DLI) can activate recipient-derived CD3+CD4-CD8- double negative T regulatory (DN Tr) cells which have a potent immune regulatory function in vitro and in vivo. Here we studied the regulatory ability of DN T cell clones generated from the spleens of nai;ve anti-L(d) transgenic TCR+ (2C x dm2)F1 mice. We were able to identify subsets of DN T cell clones that were able to kill anti-Ld CD8+ T cells, and therefore had regulatory properties, and DN T cells with no regulatory properties. Next, we investigated the ability of these in vitro generated DN T cell clones to enhance cardiac allograft survival. (2C x dm2)F1 transgenic mice were infused with either regulatory or non-regulatory DN T cell clones, or left untreated one day before receiving an Ld-mismatched cardiac grafts from (C57BL/6 x Balb/c)F1 mice. Injection of non-regulatory DN T clone cells did not prolong cardiac graft survival in (2C x dm2)F1 mice when compare to untreated controls. In contrast, all of the cardiac grafts survived more than 100 days in mice that received DN Tr clone cells prior to transplantation. These results demonstrate that DN Tr cells can be generated in vitro and protect cardiac allograft from rejection when infused into recipients prior to transplantation. They also suggest that DN Tr cells may provide a novel therapy for the treatment of allograft rejection.

Up-regulation of adenosine receptors in the cochlea by cisplatin.

In a previous study, we have demonstrated the presence of two adenosine receptor (AR) subtypes, namely A1 and A3AR, in the chinchilla cochlea. One or both of these receptors couple to activation of antioxidant enzymes, with resulting decreases in lipid peroxidation. The chemotherapeutic agent, cisplatin, was shown to produce ototoxicity within a few days of administration presumably by generating reactive oxygen species (ROS) and thereby increasing lipid peroxidation. In this study, we focused on whether lipid peroxidation induces hearing loss by assessing the cochlear antioxidant defense system over a shorter time period (24 h) following cisplatin administration. Cisplatin was administered to anesthetized chinchillas by round window membrane application and hearing loss was determined by compound action potential (CAP) and endocochlear potential (EP) 24 and 72 h post-treatment. Elevations in CAP thresholds in response to click and to 2, 4, 8 and 16 kHz tones and decreases in EP were obtained within 24 h of cisplatin treatment. These changes persisted for at least up to 72 h. Measurements of antioxidant enzymes indicate no change in the activities of superoxide dismutase, catalase or glutathione peroxidase, either 24 or 72 h following cisplatin treatment. The levels of malondialdehyde obtained at these time points were equivalent to those obtained from the controls. Furthermore, no difference in cochlear morphology was detectable by scanning electron microscopy at the basal, middle or apical turns of the cochlea within 24 h. By 72 h, however, losses in both inner and outer hair cells were observed in the basal and middle turns of the cochlea. A major finding of this study is that exposure to cisplatin led to a 5-fold up-regulation of [125I]N6-2-[4-amino-3-phenyl]ethyladenosine binding in the cochlea within 24 h, reflecting increases in expression of AR(s) in this tissue. These data indicate a dissociation between cisplatin acute (within 24 h) ototoxicity and lipid peroxidation. Furthermore, up-regulation of AR(s) may represent a rapid compensatory mechanism by the cochlea to counter the toxic effects of increased ROS generated by cisplatin.

Expression and function of adenosine receptors in the chinchilla cochlea.

Previous studies indicate the presence of adenosine receptors in the cochlear tissues obtained from different animals. This study was initiated to determine the subtypes of adenosine receptor (AR) present in the chinchilla cochlea and to assess their function. Radioligand binding studies demonstrate the presence of both the A1AR and A3AR in membranes prepared from the cochlea, using the radioligands [3H]DPCPX and [125I]APNEA. Estimates of the number (Bmax) of A1AR and A1AR plus A3AR by saturation curves were 118 +/- 13 and 417 +/- 120 fmol/mg, respectively, with the respective equilibrium dissociation constants (Kd) averaging 2.7 +/- 0.2 and 26.3 +/- 13.8 nM. No significant number of A2aAR were detected using [3H]CGS21680. The nonhydrolyzable adenosine analog R-phenylisopropyladenosine (R-PIA, 1 microM) elicited a small but significant degree of inhibition of forskolin-stimulated adenylyl cyclase activity (10.4 +/- 2.5%) in cochlear membrane preparations, which was insensitive to blockade by theophylline (100 microM). Furthermore, R-PIA elicited an increase in inositol 1,4,5-trisphosphate production in dissociated cell preparations obtained from the cochlea. No significant effect of R-PIA was observed on auditory measures such as auditory brainstem evoked response, cochlear action potential and endocochlear potential following round window application. However, round window application of R-PIA elicited significant increases in the activities of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase and significantly reduced the levels of malondialdehyde, a marker of lipid peroxidation. These results suggest a potential cytoprotective role of adenosine in the cochlea against oxidative damage.