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Masatoshi Sato,Yoshiaki Kobayashi,Takayuki Kawamata,Yukio Yasui,Kazunori Suzuki,M. Itoh,Ryoichi Kajimoto,Kazuhiko Ikeuchi,M. Arai,Phillipe Bourges 한국물리학회 2013 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.62 No.12
To identify the superconducting symmetry of Fe-based superconductors, we studied effects ofnonmagnetic-impurities on Tc, magnetic excitation spectra 00 and NMR 1/T1 − T curve, whichare sensitive to the relative signs between the order parameters on the disconnected Fermi surfacesin reciprocal space, because the symmetry is closely connected with the pairing mechanism:If the signs are opposite (symmetry S±), the mechanism is considered to be a magneticone, but when the signs are the same (symmetry S++), a novel mechanism is plausible becausethe ordinary phonon mechanism cannot realize the Tc value as high as 55 K found in Ln1111(Ln=lanthanide). Results are as follows: (a) The very small rates of Tc-suppression by impurityatoms M of LnFe1−yMyAs0.89−xF0.11+x (M=Ni, Co, Ru) can be explained only by S++. (b) The00-data for Ba(Fe, Co)2As2 (Tc 23 K) and Ca-Fe-Pt-As crystals seem to be well explained byS++ rather than by S±. (c) The nuclear magnetic resonance data can be consistently understoodby S++, too. These results suggest the S++ symmetry and a novel pairing mechanism, which canbe considered to be related to the elastic softening of C66 induced by the orbital fluctuation of thesystem.
Neurotoxicity and behavioral deficits associated with Septin 5 accumulation in dopaminergic neurons
Son, Jin H.,Kawamata, Hibiki,Yoo, Myung S.,Kim, Dae J.,Lee, Young K.,Kim, SooYoul,Dawson, Ted M.,Zhang, Hui,Sulzer, David,Yang, Lichuan,Beal, M. Flint,DeGiorgio, Lorraine A.,Chun, Hong S.,Baker, Harri Raven Press [etc.] 2005 Journal of neurochemistry Vol.94 No.4
<P>Abstract</P><P>Septin 5, a parkin substrate, is a vesicle- and membrane-associated protein that plays a significant role in inhibiting exocytosis. The regulatory function of Septin 5 in dopaminergic (DAergic) neurons of substantia nigra (SN), maintained at relatively low levels, has not yet been delineated. As loss of function mutations of parkin are the principal cause of a familial Parkinson's disease, a prevailing hypothesis is that the loss of parkin activity results in accumulation of Septin 5 which confers neuron-specific toxicity in SN-DAergic neurons. <I>In vitro</I> and <I>in vivo</I> models were used to support this hypothesis. In our well-characterized DAergic SN4741 cell model, acute accumulation of elevated levels of Septin 5, but not synphilin-1 (another parkin substrate), resulted in cytotoxic cell death that was markedly reduced by parkin co-transfection. A transgenic mouse model expressing a dominant negative parkin mutant accumulated moderate levels of Septin 5 in SN-DAergic neurons. These mice acquired a progressive <SMALL>L</SMALL>-DOPA responsive motor dysfunction that developed despite a 25% higher than normal level of striatal dopamine (DA) and no apparent loss of DAergic neurons. The phenotype of this animal, increased striatal dopamine and reduced motor function, was similar to that observed in parkin knockout animals, suggesting a common DAergic alteration. These data suggest that a threshold level of Septin 5 accumulation is required for DAergic cell loss and that <SMALL>L</SMALL>-DOPA-responsive motor deficits can occur even in the presence of elevated DA.</P>