We report the results of a 125 Te NMR study of single crystalline Pb1−xTlxTe (x=0, 0.35, 1.0%) as a window on the novel electronic states associated with the thallium impurities in PbTe. The Knight shift is enhanced as x increases, corresponding to an increase in the average density of states (DOS) coupled to a strong spatial variation in the local DOS surrounding each Tl dopant. Remarkably, for the superconducting composition (x=1.0%), the 125 Te nuclear spin relaxation rate (1/T1T ) for Te ions that are close to the Tl dopants is unexpectedly enhanced in the normal state below a characteristic temperature of ∼10 K, below which the resistivity experiences an upturn. Such a simultaneous upturn in both the resistivity and (1/T1T ) was not suppressed in the high magnetic field. We suggest that these observations are consistently accounted for by dynamical charge fluctuations in the absence of paramagnetism, which is anticipated by the charge Kondo scenario associated with the Tl dopants. In contrast, such anomalies were not detected in the non-superconducting samples (x=0 and 0.35%), suggesting a connection between dynamical valence fluctuations and the occurrence of superconductivity in Pb1−xTlxTe.

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We have performed schematic 125 Te-NMR measurements in Pb 1−x Tl x Te (x = 0, 0.35, 1.0%) and Pb 1−x Na x Te (x = 0.46, 1.45%). Superconductivity occurs above x ∼ 0.3% in Pb 1−x Tl x Te and superconducting temperature T c reaches about 1 K at x = 1.0%. In Pb 0.99 Tl 0.01 Te, the 125 Te nuclear spin relaxation rate (1/T 1 T) for Te sites near Tl dopants is unexpectedly enhanced in the normal state below a characteristic temperature of ∼ 10 K, below which the resistivity experiences an upturn. In contrast, no enhancement of 1/T 1 T is observed at low temperatures for Te sites both near and far from non-valence-skipping Na dopants in Pb 1−x Na x Te with x = 1.45%. These results suggest the existence of valence fluctuations associated with the charge Kondo effect arising from Tl dopants in the superconducting sample Pb 1−x Tl x Te with x = 1.0%.

Tribbles homolog 2 (TRIB2) functions as an adapter protein that regulates signal transductions involved in a variety of cellular functions, including tumorigenesis. However, the role of TRIB2 in the proliferation of vascular smooth muscle cells (VSMCs) and the underlying expression mechanisms remain unclear. The present study investigated the role of TRIB2 in VSMC proliferation and revealed that TRIB2 expression increases following vascular injury and platelet‐derived growth factor (PDGF)‐BB‐stimulated VSMCs. We found that pretreatment with diphenyleneiodonium (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor), U0126 (an inhibitor of mitogen‐activated protein kinase kinase 1 [MEK1]), or siRNA targeting the gene encoding early growth response 1 (EGR‐1) significantly inhibits PDGF‐BB‐induced TRIB2 expression in VSMCs. Furthermore, TRIB2 knockdown significantly inhibits PDGF‐BB‐induced proliferation of VSMCs but does not affect the phosphorylation of AKT. However, phosphorylation of ERK1 and expression of proliferating cell nuclear antibody are significantly suppressed in VSMCs by PDGF‐BB stimulation. Thus, PDGF‐BB‐induced TRIB2 expression is mediated by ROS/ERK/EGR‐1 pathways and plays a critical role in VSMC proliferation via modulation of ERK activity. We propose TRIB2 as a promising therapeutic target for the prevention of neointima formation and vascular disease.

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