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Longitudinal Magnetoresistance of Ce(Cu1−xNix)2Si2
Yoichi Ikeda,Shingo Araki,Tatsuo C. Kobayashi 한국물리학회 2013 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.63 No.3
The longitudinal magnetoresistance (LMR) of polycrystalline Ce(Cu1−xNix)2Si2 samples is investigatedbetween T = 2 and 15 K up to H = 80 kOe. The application of magnetic field inducesanomalous temperature dependence of the resistivity with the power index n < 2 for x = 0.12and 0.14, in which ρ(T) obeys a T2-law at H = 0 Oe. A sign-change of the LMR from positive(x < 0.03) to negative (x > 0.03) is observed at 2 K. The negative LMR at 80 kOe is maximized(~ −4 % at T = 2 K) around x ~ 0.10 and subsequently disappears at higher Ni concentrations. Disappearance of the positive LMR in lower x region and the negative LMR at higher Ni concentrationsimplies a collapse of a coherent Kondo lattice state, and a rapid enhancement of Kondotemperature, respectively. Anomalous quantum fluctuations are probably developed around x ~ 0.10.
Lim, Chae-Seok,Kang, Xi,Mirabella, Vincent,Zhang, Huaye,Bu, Qian,Araki, Yoichi,Hoang, Elizabeth T.,Wang, Shiqiang,Shen, Ying,Choi, Sukwoo,Kaang, Bong-Kiun,Chang, Qiang,Pang, Zhiping P.,Huganir, Richar Cold Spring Harbor Laboratory Press 2017 Genes & development Vol.31 No.6
<P>Rapid advances in genetics are linking mutations on genes to diseases at an exponential rate, yet characterizing the gene mutation-cell behavior relationships essential for precision medicine remains a daunting task. More than 350 mutations on small GTPase BRaf are associated with various tumors, and similar to 40 mutations are associated with the neurodevelopmental disorder cardio-facio-cutaneous syndrome (CFC). Wedeveloped a fast cost-effective lentivirus-based rapid gene replacement method to interrogate the physiopathology of BRaf and similar to 50 disease-linked BRaf mutants, including all CFC-linked mutants. Analysis of simultaneous multiple patch-clamp recordings from 6068 pairs of rat neurons with validation in additional mouse and human neurons and multiple learning tests from 1486 rats identified BRaf as the key missing signaling effector in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade. Moreover, the analysis creates the original big data unveiling three general features of BRaf signaling. This study establishes the first efficient procedure that permits large-scale functional analysis of human disease-linked mutations essential for precision medicine.</P>