Scanning tunneling microscopy/spectroscopy studies of two isomers of Ce@C82 on Si(111)-(7×7）surfaces

Scanning tunneling microscopy images for two isomers of Ce@C-82 were observed on Si(111)-(7x7) at 295 K. The Ce@C-82 molecules in the first layer were bound to the Si surfaces, and the motions were frozen even at 295 K. The multilayer of the Ce@C-82 isomer I (Ce@C-82-I) produced a close-packed structure in the surface layer by annealing the Si substrate at 473 K. The distance between the nearest-neighboring molecules was 1.15(4) nm whose value was consistent with that, 1.12 nm, estimated from x-ray diffraction of the Ce@C-82-I crystals. This implies that the close-packed structure is dominated by van der Waals forces, as in crystals of Ce@C-82-I. The internal structure of Ce@C-82-I was observed in the first layer due to a freeze of molecular motion caused by strong interactions between the molecule and the Si adatoms in the surface. Scanning tunneling spectroscopy revealed that the energy gaps for Ce@C-82-I and -II in the first layer opened to gap energies, E-g of 0.7 and 1.0 eV, respectively. This fact suggests that these molecules are semiconductors with smaller value of E-g than those for C-60 and C-70.</p

Scanning tunneling microscopy of Dy@C82 and Dy@C60 adsorbed on Si(111)-(7x7) surfaces

Dy@C-82 and Dy@C-60 adsorbed on Si(111)-(7x7) surface are investigated by scanning tunneling microscopy (STM) at 295 K. The Dy@C-82 molecules in the first layer are adsorbed on the Si(111)-(7x7) surface without formation of islands and nucleation, and the internal structure of the Dy@C-82 molecule is first observed on the surface at 295 K. The average heights of the Dy@C-82 molecules in the first and second layers are estimated to be 7.2 and 10.8 A, respectively, by STM. These results suggest strong interactions between the Si atoms and the Dy@C-82 molecules in the first layer. The STM image reveals that the Dy@C-60 molecule is nearly spherical, showing that the metal endohedral C-60 possesses a cage-form structure. </p

Synchrotron-radiation-stimulated etching of polydimethylsiloxane using XeF2 as a reaction gas

Synchrotron-radiation-stimulated etching of silicon elastomer polydimethylsiloxane using XeF2 as an etching gas is demonstrated

Extracellular and intraneuronal HMW-AbetaOs represent a molecular basis of memory loss in Alzheimer's disease model mouse

<p>Abstract</p> <p>Background</p> <p>Several lines of evidence indicate that memory loss represents a synaptic failure caused by soluble amyloid β (Aβ) oligomers. However, the pathological relevance of Aβ oligomers (AβOs) as the trigger of synaptic or neuronal degeneration, and the possible mechanism underlying the neurotoxic action of endogenous AβOs remain to be determined.</p> <p>Results</p> <p>To specifically target toxic AβOs <it>in vivo</it>, monoclonal antibodies (1A9 and 2C3) specific to them were generated using a novel design method. 1A9 and 2C3 specifically recognize soluble AβOs larger than 35-mers and pentamers on Blue native polyacrylamide gel electrophoresis, respectively. Biophysical and structural analysis by atomic force microscopy (AFM) revealed that neurotoxic 1A9 and 2C3 oligomeric conformers displayed non-fibrilar, relatively spherical structure. Of note, such AβOs were taken up by neuroblastoma (SH-SY5Y) cell, resulted in neuronal death. In humans, immunohistochemical analysis employing 1A9 or 2C3 revealed that 1A9 and 2C3 stain intraneuronal granules accumulated in the perikaryon of pyramidal neurons and some diffuse plaques. Fluoro Jade-B binding assay also revealed 1A9- or 2C3-stained neurons, indicating their impending degeneration. In a long-term low-dose prophylactic trial using active 1A9 or 2C3 antibody, we found that passive immunization protected a mouse model of Alzheimer's disease (AD) from memory deficits, synaptic degeneration, promotion of intraneuronal AβOs, and neuronal degeneration. Because the primary antitoxic action of 1A9 and 2C3 occurs outside neurons, our results suggest that extracellular AβOs initiate the AD toxic process and intraneuronal AβOs may worsen neuronal degeneration and memory loss.</p> <p>Conclusion</p> <p>Now, we have evidence that HMW-AβOs are among the earliest manifestation of the AD toxic process in mice and humans. We are certain that our studies move us closer to our goal of finding a therapeutic target and/or confirming the relevance of our therapeutic strategy.</p