103 research outputs found
Signature of frustrated moments in quantum critical CePdNiAl
CePdAl with Ce moments forming a distorted kagom\'e network is one of
the scarce materials exhibiting Kondo physics and magnetic frustration
simultaneously. As a result, antiferromagnetic (AF) order setting in at
~K encompasses only two thirds of the Ce moments. We
report measurements of the specific heat, , and the magnetic Gr\"uneisen
parameter, , on single crystals of CePdNiAl with
at temperatures down to 0.05~K and magnetic fields up to
~T. Field-induced quantum criticality for various concentrations is observed
with the critical field decreasing to zero at . Remarkably,
two-dimensional (2D) AF quantum criticality of Hertz-Millis-Moriya type arises
for and at the suppression of 3D magnetic order. Furthermore,
shows an additional contribution near ~T for all
concentrations which is ascribed to correlations of the frustrated one third of
Ce moments.Comment: 5+2 pages with 4+3 figure
Strong Valence Fluctuation Effects in SmAl(Ti, V, Cr)
We present a single crystal study of low temperature magnetism and transport
in SmAl ( Ti, V and Cr). Strong valence fluctuation is
manifested as Kondo effects including a large Sommerfeld coefficient ,
a weak temperature dependence of magnetic susceptibility and a
dependent resistivity. All the systems order antiferromagnetically at 6.4 K (Ti), 2.3 K (V) and 1.8 K (Cr). Systematic change in the
susceptibility, specific heat, and resistivity indicates that stronger -
hybridization in SmVAl and SmCrAl than in
SmTiAl suppresses and induces the valence fluctuations
and moreover field insensitive heavy fermion states
慢性肝炎患者における血清中および異なる3ケ所の肝組織中C型肝炎ウイルスのQuasispecies(擬均一性)の検討
取得学位:博士(医学), 学位授与番号:医博乙第1501号,学位授与年月日:平成11年10月6日,学位授与年:199
Peretinoin, an acyclic retinoid, improves the hepatic gene signature of chronic hepatitis C following curative therapy of hepatocellular carcinoma
BACKGROUND: The acyclic retinoid, peretinoin, has been shown to be effective for suppressing hepatocellular carcinoma (HCC) recurrence after definitive treatment in a small-scale randomized clinical trial. However, little has been documented about the mechanism by which peretinoin exerts its inhibitory effects against recurrent HCC in humans in vivo. METHODS: Twelve hepatitis C virus-positive patients whose HCC had been eradicated through curative resection or ablation underwent liver biopsy at baseline and week 8 of treatment with either a daily dose of 300 or 600 mg peretinoin. RNA isolated from biopsy samples was subjected to gene expression profile analysis. RESULTS: Peretinoin treatment elevated the expression levels of IGFBP6, RBP1, PRB4, CEBPA, G0S2, TGM2, GPRC5A, CYP26B1, and many other retinoid target genes. Elevated expression was also observed for interferon-, Wnt-, and tumor suppressor-related genes. By contrast, decreased expression levels were found for mTOR- and tumor progression-related genes. Interestingly, gene expression profiles for week 8 of peretinoin treatment could be classified into two groups of recurrence and non-recurrence with a prediction accuracy rate of 79.6% (P<0.05). In the liver of patients with non-recurrence, expression of PDGFC and other angiogenesis genes, cancer stem cell marker genes, and genes related to tumor progression was down-regulated, while expression of genes related to hepatocyte differentiation, tumor suppression genes, and other genes related to apoptosis induction was up-regulated. CONCLUSIONS: Gene expression profiling at week 8 of peretinoin treatment could successfully predict HCC recurrence within 2 years. This study is the first to show the effect of peretinoin in suppressing HCC recurrence in vivo based on gene expression profiles and provides a molecular basis for understanding the efficacy of peretinoin
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