In mammals, the environmental light/dark cycle strongly synchronizes the circadian clock within the suprachiasmatic nuclei (SCN) to 24 hr. It is well known that not only photic but also nonphotic stimuli can entrain the SCN clock. Actually, many studies have shown that a daytime injection of 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH DPAT), a serotonin 1A/7 receptor agonist, as a nonphotic stimulus induces phase advances in hamster behavioral circadian rhythms in vivo, as well as the neuron activity rhythm of the SCN in vitro. Recent reports suggest that mammalian homologs of the Drosophila clock gene, Period (Per), are involved in photic entrainment. Therefore, we examined whether phase advances elicited by 8-OH DPAT were associated with a change of Period mRNA levels in the SCN. In this experiment, we cloned partial cDNAs encoding hamster Per1, Per2, and Per3 and observed both circadian oscillation and the light responsiveness of Period. Furthermore, we found that the inhibitory effect of 8-OH DPAT on hamster Per1 and Per2 mRNA levels in the SCN occurred only during the hamster's mid-subjective day, but not during the early subjective day or subjective night. The present findings demonstrate that the acute and circadian time-dependent reduction of Per1 and/or Per2 mRNA in the hamster SCN by 8-OH DPAT is strongly correlated with the phase resetting in response to 8-OH DPAT.

The mechanistic cause of the dramatic activity improvement of alumina-supported silver (Ag/Al 2 O 3 ) by H 2 addition for the selective catalytic reduction of NO with propane (C 3 H 8 -SCR) was investigated by catalytic and spectroscopic studies. In situ UV-vis, in situ EXAFS, IR, and microcalorimetric experiments show that H 2 reduction of Ag + ions on Ag/Al 2 O 3 at 573 K yields protons on alumina and partially reduced Ag n δ+ clusters, which are subsequently aggregated to larger Ag clusters. During H 2 + O 2 and H 2 -assisted C 3 H 8 -SCR reactions, Ag + ions and Ag n δ+ coexist. Reoxidation with O 2 results in the redispersion of the cluster to Ag + ion, accompanying a reaction of protons. The relationship between cluster size, redox properties, and catalytic activity is examined using Ag/Al 2 O 3 of different Ag loadings. The steady-state NO reduction rate correlates fairly well with the amount of Ag n δ+ during the H 2 -assisted C 3 H 8 -SCR reaction. It is shown that Ag n δ+ is the active species, whereas monomeric Ag + ion and metallic Ag particles are inactive. With Ag loading, the Ag + reduction rate increases and the rate of cluster reoxidation decreases. A balance between the rate of reduction and reoxidation of Ag species is an important factor that controls the size and oxidation state of the Ag species and consequently the catalytic activity of Ag/Al 2 O 3 . ESR has provided evidence, for the first time, for the in situ generation of superoxide ions in H 2 + O 2 and H 2 -assisted C 3 H 8 -SCR reactions. The comprehensive reason for the hydrogen effect in HC-SCR is discussed, focusing on the role of the cluster and protons on the reductive O 2 activation to superoxide ion.

The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.