In this study, we conducted various magnetotransport measurements on Fe 1+y Te 1−x Se x single crystals from which excess iron was sufficiently removed. Our results revealed that crossover from the incoherent to the coherent electronic state and opening of the pseudogap occur at high temperatures (≈ 150 K for x = 0.2). This is accompanied by a more substantial pseudogap and the emergence of a phase with a multi-band nature at lower temperatures (below ≈ 50 K for x = 0.2) before superconductivity sets in. A comparison of these results with those of the as-grown (non-superconducting) samples implies that the coherent state accompanied by the pseudogap is needed for the occurrence of superconductivity in this system. arXiv:1904.13020v1 [cond-mat.supr-con]
Using a laser-excited angle-resolved photoemission spectroscopy capable of bulk sensitive and high-energy resolution measurements, we reveal a new phenomenon of superconductors in the optimally doped trilayer Bi_{2}Sr_{2}Ca_{2}Cu_{3}O_{10+δ}. We observe a hybridization of the Bogoliubov bands derived from the inner and outer CuO_{2} planes with different magnitudes of energy gaps. Our data clearly exhibit the splitting of coherent peaks and the consequent enhancement of spectral gaps. These features are reproduced by model calculations, which indicate that the gap enhancement extends over a wide range of Fermi surface up to the antinode. The significant modulation of electron pairing uncovered here might be a crucial factor to achieve the highest critical temperature in the trilayer cuprates.
PK-120 is a substrate for plasma kallikrein (PK), recently purified from human plasma. Here we have established the cDNA sequence for human PK-120 mRNA. The deduced amino sequence of PK-120 revealed that it consists of 902 amino acid residues with a calculated mass of 116,423 Da. The putative cleavage sites by PK have been proposed, suggesting that PK-120 may be a precursor of a bioactive peptide. Most interestingly, PK-120 showed significant sequence identities to heavy chains (HCs) of the inter-alpha-trypsin inhibitor (ITI) superfamily.
We previously generated a rat model that spontaneously developed small vessel vasculitis (SVV). In this study, a T cell clone reactive with rat vascular endothelial cells (REC) was established and named VASC-1. Intravenous injection of VASC-1 induced SVV in normal recipients. VASC-1 was a TCRαβ/CD3-positive CD4/CD8 double-negative T cell clone with expression of NKG2D. The cytokine mRNA profile under unstimulated condition was positive for IL-4 and IFN-γ but negative for IL-2 and IL-10. After interaction with REC, the mRNA expression of IL-2, IL-5 and IL-6 was induced in VASC-1, which was inhibited by blocking of CD1d on the REC surface. Although the protein levels of these cytokines seemed to be lower than the detection limit in the culture medium, IFN-γ was detectable. The production of IFN-γ from the VASC-1 stimulated with LPS-pre-treated REC was inhibited by the CD1d blockade on the REC. These findings indicated VASC-1 as an NKT cell clone. The NKT cell pool includes two major subsets, namely types I and II. Type I NKT cells are characterized by expression of semi-invariant TCRs and the potential to bind to marine sponge-derived α-galactosylceramide (α-GalCer) loaded on CD1d; whereas, type II NKT cells do not manifest these characteristics. VASC-1 exhibited a usage of TCR other than the type I invariant TCR α chain and did not bind to α-GalCer-loaded CD1d; therefore, it was determined as a type II NKT cell clone. The collective evidence suggested that REC-reactive type II NKT cells could be involved in the pathogenesis of SVV in rats.
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