No abstract

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.

Serratia marcescens 2170 produces three different types of chitinases and chitin-binding protein CBP21. We found that transposon insertion into the 5' untranslated region (5' UTR) of chiPQ-ctb led to defective chitinase and CBP21 production. ChiX small RNA possessed the complementary sequence of the 5' UTRs of the chiPQ-ctb and chiR and repressed the expression of chiP and chiR. ChiX was detected in a medium containing glucose, glycerol, GlcNAc, and (GlcNAc)2, but the expression of both chiP and chiR was only observed in a medium containing (GlcNAc)2. ∆chiX mutant produced chitinases, CBP21, and chitobiase without induction. chiP transcripts were more abundant than those of chiR or chiX in a medium containing (GlcNAc)2. These results suggest that the constitutively expressed ChiX binds to the highly abundant chiP 5' UTR, thereby leading to the induction of chiR mRNA translation and the subsequent expression of chitinases and CBP21.

The cross-sectional association of blood pressure with urinary sodium and potassium excretion was investigated with a stepwise regression analysis. Spot urine of 7441 females between 40 and 69 years was collected from 169 municipalities (88 urban and 81 rural) covering all prefectures in Japan. The filter paper sampling technique for urine was used to collect samples of subjects from March to December in 1985. Spot urine samples were analyzed for sodium, potassium and creatinine. In addition, 24-hr sodium and potassium excretions were estimated by predictive equations. Blood pressure, sodium excretion and sodium/potassium ratios were higher in rural areas than in urban areas. Consistent positive correlations between urinary sodium and blood pressure, and negative correlations between urinary potassium and blood pressure were observed in the whole country of Japan, in both urban and rural areas, and also in separate observations of twelve regions in Japan with some exceptions. When compared in standardized partial regression coefficients, relative effects of potassium on systolic blood pressure were higher than those of sodium in the whole of Japan, in urban and rural areas, and in five among the twelve regions. The present Japanese study confirmed a positive within-population relationship between sodium excretion and blood pressure and a negative relationship between potassium excretion and blood pressure.

It has long been discussed whether endogenous retroviruses (ERVs) are involved in the pathogenesis of autoimmune diseases. Among various human endogenous retroviruses (HERVs), we have focused on HERV-R. To investigate the biological roles of HERV-R, we earlier established transgenic rats carrying the full sequence of the viral genome. In these HERV-R rats, however, no disease occurred. Another trigger that induces autoimmunity may be essential for the recognition of HERV-R products by the immune system. Thus, in this study, we mated HERV-R rats with env-pX rats (transgenic rats carrying the env-pX gene of human T cell leukemia virus type I) that develop autoimmune diseases, and generated double transgenic (DTG) rats. In DTG rats, autoimmune diseases occurred similarly in env-pX rats. Interestingly, deposition of rat IgM but not IgG was observed on the glomerular endothelial cells. Such IgM deposition was never seen in the parental HERV-R or env-pX rats. We considered that in situ formation of immune complexes consisted of the HERV-R env glycoprotein and anti-HERV-R env IgM antibodies (Abs) in DTG rats, according to the following evidence: (1) No dense deposit, representing deposition of circulating immune complexes, was seen on glomerular endothelial cells. (2) IgM Abs reactive with HERV-R env glycoprotein were generated in the serum. (3) HERV-R env glycoprotein was expressed in the kidney, specifically on glomerular endothelial cells. (4) IgM deposition was partly colocalized with the HERV-R env glycoprotein on the glomeruli. These findings strongly suggest that the HERV-R env glycoprotein is recognized as an autoantigen in the host with autoimmune diseases.