527 research outputs found

    In-plane Anisotropy on Resistivity and Thermopower in The Misfit Layered Oxide Bi2-xPbxSr2Co2Oy

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    We investigated the in-plane anisotropy on the resistivity and thermopower of Bi2-xPbxSr2Co2Oy single crystals, which have a misfit structure between the hexagonal CoO2 layer and the rock salt Bi2Sr2O4 layer. The resistivity and thermopower show significantly large anisotropy, which exceeds two at maximum. This anisotropy would come from the anisotropic pseudogap formation enhanced by the misfit structure. The thermopower changes with Pb doping to take a maximum at x=0.4. The misfit structure improves the thermoelectric properties through chemical pressure. The power factor is as large as 9 muW/cmK2 at 100 K for x=0.6, which is the highest value for thermoelectric oxides at 100 K.Comment: 4 pages, 3 figures, submitted to Jpn. J. Appl. Phy

    Thrombocytopenia in Preterm Infants with Intrauterine Growth Restriction

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    Sick preterm infants often have thrombocytopenia at birth, and this is often associated with intrauterine growth restriction (IUGR), or birth weights less than the 10th percentile. The pathogenesis of the thrombocytopenia and its importance in IUGR are still unclear. We studied the characteristics of preterm IUGR infants with thrombocytopenia. Twenty-seven singleton Japanese preterm IUGR infants were born between January 2002 and June 2007 at Okayama University Hospital. Infants with malformation, chromosomal abnormalities, alloimmune thrombocytopenia, sepsis, and maternal aspirin ingestion were excluded. The infants were divided into group A (n&#65309;8), which had thrombocytopenia within 72h after birth, and group B (n&#65309;19), which did not. There were significant differences in birth weight, head circumference, umbilical artery (UA)-pulsatility index (PI), middle cerebral artery-PI, UA-pH, UA-pO2, and UA-pCO2. The infants in group A were smaller, had abnormal blood flow patterns, and were hypoxic at birth. We speculate that the infants with thrombocytopenia were more severely growth-restricted by chronic hypoxia. Thrombocytopenia is an important parameter for chronic hypoxia in the uterine.</p

    Protective effect of lipoproteins containing apoprotein A-I on Cu2+ - catalyzed oxidation of human low density lipoprotein

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    AbstractTwo apoprotein A-I (apoA-I)-containing lipoproteins, one containing apoA-I and apoA-II (LpA-I/A-II) and the other containing only apoA-I (LpA-I), were examined for their effect on Cu2+-mediated oxidation of low density lipoprotein (LDL). The presence of LpA-I or LpA-I/A-II prevented LDL oxidation when assessed by the electrophoretic mobility, apoprotein B fragmentation and amounts of thiobarbituric acid-reactive substances. The protection of LDL oxidation by these lipoproteins was effective for up to 6 h, with LpA-I being more active than LpA-I/A-II. Results from these in vitro model experiments raise a possibility that LpA-I mayplay a role in protecting LDL from Cu2+ -mediated oxidation

    Identification of a single base insertion in the COL4A5 gene in Alport syndrome

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    Identification of a single base insertion in the COL4A5 gene in Alport syndrome. We identified a novel mutation in the COL4A5 gene of a Japanese patient with Alport syndrome. A combination of in vitro amplification of the exons with single strand conformation polymorphisms (SSCP) analysis suggested the presence of a mutation in exon 48. Sequencing of the amplified DNA revealed a single base (T) insertion which was between nucleotides T 4750 and G 4751 within the methionine 1516. This mutation caused a shift in the reading frame of nine amino acids and introduced a premature termination signal that would be expected to lack about two-thirds of the noncollagenous (NCI) domain. This mutation may interfere with type IV collagen assembly leading to increased permeability and play a causative role in the glomerular basement membrane abnormality of this patient with typical Alport syndrome. Gene tracking by restriction enzyme NlaIII digestion revealed that the patient's mother is heterozygous whereas the patient's brother and one sister are normal, albeit they have hematuria and proteinuria. Without gene analysis, they would have been misdiagnosed. We propose that the diagnosis of Alport syndrome should be made on the basis of both clinical phenotypes and molecular defects
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