No abstract

Au@Ag core-shell nanocrystals have been synthesized by using a microwave-polyol method, and their growth mechanisms have been studied. When HAuCl 4 ‚4H 2 O was reduced in ethylene glycol in the presence of poly(vinylpyrrolidone) (PVP) as a polymer surfactant, a mixture of triangular twin platelike, octahedral, and multiple-twinned decahedral Au nanocrystals, having only {111} facets, was prepared. When Ag + was reduced by using these Au nanocrystals as seeds, triangular-bipyramidal, cubic, and rod/wire Ag shells, having {100} facets, were overgrown, respectively. It was concluded that morphology changes between Au cores and Ag shells arise from changes in the adsorption selectivity of PVPs from {111} facets of Au to {100} facets of Ag. Total space volumes of Ag shells overgrown on Au cores were on the order of cubes > triangular-bipyramidal crystals > rods and wires. These findings provide general information on the growth mechanism of face-centered cubic (FCC) types of single crystals in the presence of a polymer surfactant, which is difficult to obtain from monometallic crystals.

The fatty acid (FA) docosahexaenoic acid (DHA, 22: 6n-3) is highly enriched in membrane phospholipids of the central nervous system and retina. Loss of DHA because of n-3 FA deficiency leads to suboptimal function in learning, memory, olfactory-based discrimination, spatial learning, and visual acuity. G protein-coupled receptor (GPCR) signal transduction is a common signaling motif in these neuronal pathways. Here we investigated the effect of n-3 FA deficiency on GPCR signaling in retinal rod outer segment (ROS) membranes isolated from rats raised on n-3-adequate or -deficient diets. ROS membranes of second generation n-3 FA-deficient rats had ϳ80% less DHA than n-3-adequate rats. DHA was replaced by docosapentaenoic acid (22:5n-6), an n-6 FA. This replacement correlated with desensitization of visual signaling in n-3 FA-deficient ROS, as evidenced by reduced rhodopsin activation, rhodopsintransducin (G t ) coupling, cGMP phosphodiesterase activity, and slower formation of metarhodopsin II (MII) and the MII-G t complex relative to n-3 FA-adequate ROS. ROS membranes from n-3 FA-deficient rats exhibited a higher degree of phospholipid acyl chain order relative to n-3 FA-adequate rats. These findings reported here provide an explanation for the reduced amplitude and delayed response of the electroretinogram a-wave observed in n-3 FA deficiency in rodents and nonhuman primates. Because members of the GPCR family are widespread in signaling pathways in the nervous system, the effect of reduced GPCR signaling due to the loss of membrane DHA may serve as an explanation for the suboptimal neural signaling observed in n-3 FA deficiency.

L-ascorbic acid (vitamin C) is one of the well-known anti-viral agents, especially to influenza virus. Since the in vivo anti-viral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-α/β, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-α/β, were increased in the lung. Taken together, vitamin C shows in vivo anti-viral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-α/β.