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Lactoferrin (LF) has been implicated in innate immunity. Here we reveal the signal transduction pathway responsible for human LF (hLF)-triggered nuclear factor-kappaB (NF-kappaB) activation. Endotoxin-depleted hLF induces NF-kappaB activation at physiologically relevant concentrations in the human monocytic leukemia cell line, THP-1, and in mouse embryonic fibroblasts (MEFs). In MEFs, in which both tumor necrosis factor receptor-associated factor 2 (TRAF2) and TRAF5 are deficient, hLF causes NF-kappaB activation at a level comparable to that seen in wild-type MEFs, whereas TRAF6-deficient MEFs show significantly impaired NF-kappaB activation in response to hLF. TRAF6 is known to be indispensable in leading to NF-kappaB activation in myeloid differentiating factor 88 (MyD88)-dependent signaling pathways, while the role of TRAF6 in the MyD88-independent signaling pathway has not been clarified extensively. When we examined the hLF-dependent NF-kappaB activation in MyD88-deficient MEFs, delayed, but remarkable, NF-kappaB activation occurred as a result of the treatment of cells with hLF, indicating that both MyD88-dependent and MyD88-independent pathways are involved. Indeed, hLF fails to activate NF-kappaB in MEFs lacking Toll-like receptor 4 (TLR4), a unique TLR group member that triggers both MyD88-depependent and MyD88-independent signalings. Importantly, the carbohydrate chains from hLF are shown to be responsible for TLR4 activation. Furthermore, we show that lipopolysaccharide-induced cytokine and chemokine production is attenuated by intact hLF but not by the carbohydrate chains from hLF. Thus, we present a novel model concerning the biological function of hLF: hLF induces moderate activation of TLR4-mediated innate immunity through its carbohydrate chains; however, hLF suppresses endotoxemia by interfering with lipopolysaccharide-dependent TLR4 activation, probably through its polypeptide moiety.

The presence of intergrowths in the Sr 3 V 2 O 7 compound has been elucidated by means of high resolution transmission electron microscopy and several types of atomic stacking sequence of the intergrowths, i.e. a stacking irregularity along the c direction of Sr 3 V 2 O 7 , have been clarified. The intergrowths were composed of the Sr 4 V 3 O 10 phase, i.e. one of the related compounds Sr n +1 V n O 3 n +1 . The presence of such intergrowths are considered to be produced by matrix compositional fluctuations.

The continuously varying solid solution in the Bi2+xSr2−xCaCu2O8+δ system has been clarified within the range −0.1

Farnesoid X receptor (FXR), a member of the nuclear receptor superfamily, has been shown to play pivotal roles in bile acid homeostasis by regulating the biosynthesis, conjugation, secretion and absorption of bile acids. Accumulating data suggest that FXR signaling is involved in the pathogenesis of liver and metabolic disorders. Here we show that FXR expression is significantly suppressed in HepG2 cells exposed to hypoxia. Concomitantly, the expression of the bile salt export pump, known as an FXR target gene product and responsible for the excretion of bile acids from the liver, is also decreased under hypoxia. Overexpression of hypoxia-inducible factor (HIF)-1alpha does not mimic the suppressive effect of hypoxia on FXR expression. Furthermore, simultaneous knockdown of HIF-1alpha, HIF-2alpha and HIF-3alpha fails to restore the FXR expression level under hypoxia, indicating that HIF is not involved in hypoxia-evoked FXR downregulation. Instead, we demonstrate that p38 mitogen-activated protein kinase is an indispensable factor for FXR downregulation under hypoxia. Thus, we propose a novel liver disorder model in which two signaling molecules, p38 mitogen-activated protein kinase and FXR, may contribute to the linkage of two pathogenic conditions, i.e. ischemia, a condition accompanying hypoxia, and cholestasis, a condition with intrahepatic accumulation of cytotoxic bile acids.

X-ray lattice parameter measurements of the Bi2-x (Sr,Ca)3-yCu2-zO8+d system show that a continuously varying solid-solution cation nonstoichiometry exists within the overall composition ranges x < 0.32, -0.2 < y < 0.32, and z < 0.25. A modulated structure along the b axis remains present over these composition ranges. Defects introduced by cation deficiency have been clarified to be vacancies by density measurements. The oxygen content determined by titration decreases proportionately with increasing cation vacancy concentrations. In Bi-deficient compositions, the interstitial oxygen ion concentration decreased and the oxygen vacancy concentration increased with increasing concentration of Bi vacancies. The critical temperature, Tc, shows a maximum value at the stoichiometric cation composition and decreases to a slightly lower (5 to 10 K) constant value across the nonstoichiometric composition region with both increasing alkaline-earth and Cu deficiency.

The authors have discovered a new polytypic Sr4V3O10−x phase and have proposed structural models for this phase, which can be obtained by introducing double VO layers in an ordinary Sr2VO4 phase. The atomic stacking difference along the c-direction between the ordinary Sr4V3O10 phase and the new phase is discussed.

Zr–Hf interdiffusions were carried out at 1350° to 1520°C for polycrystalline tetragonal solid solutions of 14CeO2·86(Zr1-xHfx)O2 with X= 0.02 and 0.10. Lattice and grain-boundary interdiffusion parameters were calculated from the concentration distributions by using Oishi and Ichimura's equation. Lattice interdiffusion coefficients were described by D= 3.0 × 103 exp[-623 (kJ/mol)/RT] cm2/s and grain-boundary interdiffusion parameters by δD' = 0.29 exp[-506 (kJ/mol)/RT] cm3/s. The cation diffusivity was lower than the anion diffusivity. The results were compared with diffusivities in the fluorite-cubic solid solution. The critical grain radii for stabilization of the tetragonal phase in CeO2-doped ZrO2 were 11 and 6 μm for the solutions with 2 and 10 mol% HfO2 substitution, respectively, both of which are much greater than in the Y2O3-doped ZrO2 solid solution.

Intracellular accumulation of denatured proteins impairs cellular function. The proteasome is recognized as an enzyme responsible for the effective clearance of those cytotoxic denatured proteins. As another enzyme that participates in the destruction of damaged proteins, we have identified oxidized protein hydrolase (OPH) and found that OPH confers cellular resistance to various kinds of oxidative stress. In this study, we demonstrate the roles of the proteasome and OPH in the clearance of denatured proteins. The inhibition of proteasome activity results in the elevation of protein carbonyls in cells under oxidative stress. On the other hand, cells overexpressing OPH retain higher resistance to oxidative stress, even though the proteasome activity is inhibited. Furthermore, upon inhibition of the proteasome activity, OPH is recruited to a novel organelle termed the aggresome where misfolded or denatured proteins are processed. Thus, OPH and the proteasome coordinately contribute to the clearance of cytotoxic denatured proteins.

The present study was undertaken to know the effect of supplementation of fish oil with high n-3 polyunsaturated fatty acids (PUFA) on oxidative stress-induced DNA damage of rat liver in vivo. Male Wistar rats were fed a diet containing fish oil or safflower oil with high n-6 PUFA at 50 g/kg of diet and an equal amount of vitamin E at 59 mg/kg of diet for 6 weeks. Livers of rats fed fish oil were rich in n-3 PUFA, whereas those of rats fed safflower oil were rich in n-6 PUFA. Ferric nitrilotriacetate was intraperitoneally injected to induce oxidative stress. The degree of lipid peroxidation of the liver was assessed by the levels of phospholipid hydroperoxides and thiobarbituric acid-reactive substances (TBARS), and the degree of oxidative DNA damage was assessed by comet type characterization in alkaline single-cell gel electrophoresis and 8-hydroxy-2'-deoxyguanosine levels. The levels of TBARS of the livers of the fish oil diet group increased to a greater extent than those of the safflower oil diet group, whereas the levels of the hydroperoxides of the livers of both diet groups increased to a similar extent. The vitamin E level of livers of the fish oil diet group was remarkably decreased. The degree of DNA damage of both diet groups was increased, but the increased level of the fish oil diet group was remarkably lower than that of the safflower oil diet group. The above results indicate that fish oil supplementation does not enhance but appears to protect against oxidative stress-induced DNA damage and suggest that lipid peroxidation does not enhance but lowers the DNA damage.

The effect of supplementation of n-3 polyunsaturated fatty acids (PUFA) on oxidative stress-induced DNA damage of rat hepatocytes was examined. Male Wistar rats were fed a diet containing safflower oil (control n-6 PUFA diet) or fish oil (n-3 PUFA diet) in 50 g/kg of dried diet and an equal amount of vitamin E in 59 mg/kg of dried diet for 6 weeks. The liver of rats fed safflower oil was rich in n-6 PUFA, whereas that of rats fed fish oil was rich in n-3 PUFA. Isolated hepatocytes were treated in vitro with ADP/Fe (II) ion or hydrogen peroxide at 37 degrees C for 30 min to induce oxidative stress. The degree of lipid peroxidation was assessed by the levels of phospholipid hydroperoxides and thiobarbituric acid-reactive substances. The degree of oxidative DNA damage was assessed based on comet-type characterization in alkaline single-cell gel electrophoresis and 8-hydroxy-deoxyguanosine levels. In both ADP/Fe(II) ion and hydrogen peroxide oxidation, the degree of lipid peroxidation of hepatocytes increased in both diet groups, and the level of increase in the fish oil diet group was slightly higher than that in the safflower oil diet group. In ADP/Fe(II) ion oxidation, the degree of DNA damage increased in both diet groups, but there were no significant differences in the level of increase. In contrast, in hydrogen peroxide oxidation, the degree of DNA damage increased in both diet, and the increase in the fish oil diet group was significantly lower than that in the safflower oil diet group. It is unlikely that an n-3 PUFA-rich diet enhances oxidative stress-induced hepatocyte DNA damage as compared with the control n-6 PUFA-rich diet.

Hypocholesterolemic activity of dietary polyunsaturated fatty acids is observed after relatively short-term but not long-term feedings, and their long-term feedings are suspected to accelerate aging through tissue accumulation of lipid peroxides and age pigments (lipofuscin). To define the long-term effects of fats and oils in more detail, female mice were fed a conventional basal diet supplemented with lard (Lar), high-linoleic (n-6) safflower oil (Saf), rapeseed oil (Rap), high-alpha-linolenic (n-3) perilla oil (Per), or a mixture of ethyl docosahexaenoate and soybean oil (DHA/Soy) from 17 weeks to 71 weeks of age. The DHA/Soy and Per groups had decreased serum cholesterol levels compared with the Lar and Saf groups, but the difference between the Lar and Saf groups was not significant. The 3-hydroxy-3-methyglutary-CoA (HMG-CoA) reductase activity in the liver was also significantly lower in the Per and DHA/Soy groups. However, no significant difference in lipofuscin contents in the brain and liver was observed among the 5 dietary groups, despite significant differences in peroxidizability indices of the dietary and/or tissue lipids. These results indicate that n-3 fatty acid-rich oils are hypocholesterolemic by suppressing hepatic HMG-CoA reductase activity compared with animal fats and high-linoleic (n-6) oil, but tissue lipofuscin contents are not affected by a long-term feeding of fats and oils with different degree of unsaturation in mice.

Oxidized protein hydrolase (OPH) preferentially degrades oxidatively damaged proteins in vitro and is widely distributed in various cells and tissues. The role of OPH in intact cells exposed to oxidative stress was examined. For this purpose, using COS-7, a cell line derived from African green monkey kidney, COS-7-OPH cells that stably overexpressed OPH were established. When COS-7-OPH cells were exposed to oxidative stress induced by H(2)O(2) and paraquat, accumulation of protein carbonyls in the cells was apparently lower than that of parental COS-7 cells, and COS-7-OPH cells were significantly resistant to the oxidative stress compared with parental COS-7 cells. The majority of overexpressed OPH in the cells was found to be located uniformly in cytosol, and its location was not altered by H(2)O(2)-induced oxidative stress. Above results indicate that OPH in intact cells plays a preventive role against oxidative stress and suggest that OPH relieves cells from accumulation of oxidatively damaged proteins.

We investigated whether free Fe ions were released in erythrocytes during aging process in the circulation. Young and senescent erythrocytes were separated from freshly drawn human blood by Percoll density gradient centrifugation. Two different methods were employed for determination of free Fe ions in erythrocytes, desferrioxamine (DFO) method and bleomycin method. DFO-chelatable Fe ions were detected in whole erythrocytes from 2 donors, and the DFO-chelatable free Fe ion levels in senescent erythrocytes were higher than those in young erythrocytes. Bleomycin-sensitive Fe ions, which was rather lower than DFO-chelatable Fe ions, were also detected in whole erythrocytes from 5 donors, and the free Fe ion levels in senescent erythrocytes were also higher than those in young erythrocytes. Free Fe ions may be derived from oxidative damage of hemoglobin, because treatment of whole erythrocytes or purified oxyhemoglobin with hydrogen peroxide gave increased free Fe ions. The results indicated that free Fe ions were released from erythrocytes during aging process in the circulation. Released free Fe ions would promote oxidative damages of the cells during aging process.

NMR measurements have been made to study the electron correlation effect in metallic layered perovskite compounds Sr n +1 V n O 3 n +1 ( n =2, 3 and ∞). It has been found that the exchange enhancement of the spin susceptibil ity increases with decreasing n from ∞ to 2 within the random phase approximation.

Zr-Hf interdiffusion was studied in the temperature range of 1,650 to 1,850C in air for polycrystalline fluorite-cubic systems of 90CeO[sub 2] [center dot] 10(Zr[sub 1 [minus]x]Hf[sub x])O[sub 2] and 60CeO[sub 2] [center dot] 40(Zr[sub 1 [minus]x]Hf[sub x])O[sub 2]. Lattice and grain-boundary diffusion parameters were calculated from the Zr-Hf concentration distributions by using the grain-boundary diffusion equation of Oishi and Ichimura. The cation lattice diffusivity was close to that in the fluorite-cubic Y[sub 2]O[sub 3]-ZrO[sub 2] solid solution.

PURPOSE: There is growing evidence that tumor-specific immune responses play an important role in anti-cancer therapy, including radiotherapy. Using mouse tumor models we demonstrate that irradiation-induced anti-tumor immunity is essential for the therapeutic efficacy of irradiation and can be augmented by modulation of cytotoxic T lymphocyte (CTL) activity. METHODS AND MATERIALS: C57BL/6 mice, syngeneic EL4 lymphoma cells, and Lewis lung carcinoma (LL/C) cells were used. Cells were injected into the right femurs of mice. Ten days after inoculation, tumors were treated with 30 Gy of local X-ray irradiation and their growth was subsequently measured. The effect of irradiation on tumor growth delay (TGD) was defined as the time (in days) for tumors to grow to 500 mm3 in the treated group minus that of the untreated group. Cytokine production and serum antibodies were measured by ELISA and flow cytometry. RESULTS: In the EL4 tumor model, tumors were locally controlled by X-ray irradiation and re-introduced EL4 cells were completely rejected. Mouse EL4-specific systemic immunity was confirmed by splenocyte cytokine production and detection of tumor-specific IgG1 antibodies. In the LL/C tumor model, X-ray irradiation also significantly delayed tumor growth (TGD: 15.4 days) and prolonged median survival time (MST) to 59 days (versus 28 days in the non-irradiated group). CD8(+) cell depletion using an anti-CD8 antibody significantly decreased the therapeutic efficacy of irradiation (TGD, 8.7 days; MST, 49 days). Next, we examined whether T cell modulation affected the efficacy of radiotherapy. An anti-CTLA-4 antibody significantly increased the anti-tumor activity of radiotherapy (TGD was prolonged from 13.1 to 19.5 days), while anti-FR4 and anti-GITR antibodies did not affect efficacy. CONCLUSIONS: Our results indicate that tumor-specific immune responses play an important role in the therapeutic efficacy of irradiation. Immunomodulation, including CTLA-4 blockade, may be a promising treatment in combination with radiotherapy.

Human T-lymphoid cell line Jurkat cells were mildly oxidized with diamide, hydrogen peroxide, or t-butyl-hydroperoxide. The recognition of Jurkat cells in the absence of serum by human monocytic leukemia cell line THP-1 differentiated into macrophages was enhanced by the oxidation with these reagents. The recognition was maximal when Jurkat cells were treated with each of the reagents at the relatively low concentrations, and the recognition was decreased on treatment with the reagents at the higher concentrations. The enhanced recognition of THP-1 macrophages to diamide-oxidized Jurkat cells was lowered when the binding was conducted in the presence of the oligosaccharides from band 3 glycoprotein and lactoferrin. The inhibitory effect of band 3 oligosaccharides was abolished by removal of the non-reducing-terminal sialyl residues or by cleavage of poly-N-acetyllactosaminyl sugar chains in the saccharides. Moreover, on enzymatic removal of the non-reducing-terminal sialyl residues or enzymatic cleavage of the poly-N-acetyllactosaminyl sugar chains on the surface of Jurkat cells prior to oxidation, the cells were recognized poorly by THP-1 macrophages. Human naturally occuring antiband 3 IgG bound effectively to the hydrogen peroxide-oxidized Jurkat cells. This binding was abolished by the enzymatic cleavage of the poly-N-acetyllactosaminyl sugar chains on the surface of the cells prior to oxidation with hydrogen peroxide. The results indicate that binding of THP-1 macrophages and antiband 3 IgG to Jurkat cells was increased by mild oxidation of Jurkat cells, and the bindings were through sialylated poly-N-acetyllactosaminyl sugar chains on Jurkat cell surface.

We have investigated the relationship between the microstructures and pinning forces by measuring the magnetic‐field dependence and angular dependence of Jc in several kinds of YBCO thin films having different microstructures. A high‐Jc value was kept even when the magnetic field was applied perpendicular to the film plane in the case of a c‐axis‐oriented film which was studded with a‐axis‐oriented grains. The boundaries between the a‐axis‐oriented grain and the c‐axis‐oriented grain are considered to be effective as pinning centers.

Human T-lymphoid cell line Jurkat was treated with actinomycin D (ActD) and cycloheximide (CHX). The induction of apoptosis was confirmed by the chromatin condensation and DNA ladder fragmentation. Anti-band 3 IgG, purified from normal human plasma, bound to the ActD- or CHX-treated cells, and the binding was correlated to the degree of apoptosis. Antioxidants, N -acetylcysteine, pilloridine dithiocarbamate, and trolox, inhibited neither induction of DNA fragmentation of ActD-treated cells nor anti-band 3 IgG binding to ActD-treated cells, indicating that formation of the anti-band 3 IgG binding sites on the apoptotic cell surface is caused by nonoxidative mechanism. When Jurkat cells were treated with endo-β-galactosidase to cleave sialylated poly- N -acetyllactosaminyl saccharide chains from the cell surface before induction of apoptosis, the binding of anti-band 3 IgG was abolished. The results indicate that sialylated poly- N -acetyllactosaminyl saccharide chains on the cell surface are requisite for the binding of anti-band 3 IgG to apoptotic cells.

4-Hydroxy-2(or 5)-ethyl-5(or 2)-methyl-3(2H)-furanone (HEMF) is representative of the Maillard reaction-derived reductones found in many foodstuffs. Influence of HEMF on iron ion-induced oxidative modification of human erythrocyte membranes and low density lipoprotein (LDL) under aerobic conditions was investigated. When human erythrocytes were incubated at 37 degrees C for 24 h with HEMF alone, levels of thiobarbituric acid-reactive substances (TBARS) and non-ionic detergent C12E8-insoluble membrane protein aggregates in the membranes were unchanged. Levels of TBARS and protein aggregates in the membranes increased on treatment of the cells with Fe(III) ion at 37 degrees C for 3 h were lowered in the presence of HEMF. Western blot analysis indicated that aggregates of band 3 protein induced by Fe (III) ion were decreased in the presence of HEMF, and the level of TBARS in LDL increased on treatment with Fe(II) or Fe(II) ion at 37 degrees C for 24 h was also lowered in the presence of HEMF. The results indicate that HEMF protected the iron ion-induced oxidative modification of human erythrocyte membranes and LDL.

Erythrocytes oxidized or aged in the circulation undergo membrane protein aggregation and anti-band 3 autoantibody binding to the cell surface. When human erythrocytes were mildly oxidized in vitro with 0.1 mM Fe(III) at 37 degrees C for 3 h, the aggregation of nonionic detergent C(12)E(8)-insoluble membrane protein and the binding of anti-band 3 IgG to the cell surface were increased. Incubation of membranes isolated from the oxidized cells increased the amount of protein aggregates by 5-fold after 6 h, while incubation for a further 12 h sharply decreased the amount of aggregates. In the presence of diisopropyl fluorophosphate (DFP), however, the increased amount of aggregates was maintained in the subsequent incubation. Western blot analysis of the aggregates using rabbit anti-band 3 showed that band 3 protein aggregates increased in the initial stage of incubation and decreased upon subsequent incubation, whereas the increased band 3 protein aggregates did not subsequently decrease when membranes were incubated in the presence of DFP. Incubation of the oxidized cells at 37 degrees C for 18 h caused reduction of the membrane protein aggregates and the (125)I-anti-band 3 IgG binding to the cell surface, while incubation in the presence of DFP did not cause these reductions. The results suggest that the oxidation-induced cell membrane protein aggregates were probably removed by 80-kDa serine protease, namely, oxidized protein hydrolase (OPH), in the oxidized cell membranes [Fujino et al. (1998) Biochim. Biophys. Acta 1374, 47-54; (1998) J. Biochem. 124, 1077-1085; (2000) Biochim. Biophys. Acta 1478, 102-112], and as a result the increased anti-band 3 binding to the cell surface was reduced.

Nitrotyrosine is considered a stable biomarker of reactive nitrogen species, including nitrogen dioxide (NO2) and peroxynitrous acid (ONOOH) in biomaterials. There are inconsistent observations on the detection of free and protein-associated nitrotyrosine in normal human plasma. Human erythrocytes, differentiated from erythrocyte precursor cells in the bone marrow, circulating in the body for an average of 120 d, and finally removed by spleen macrophages, may be exposed to reactive nitrogen species. In the present study, membrane proteins and hemoglobin from the senescent erythrocyte population were compared with those from young erythrocytes separated from the same individuals in their nitrotyrosine presence using newly prepared rabbit polyclonal anti-nitrotyrosine-ribonuclease A and anti-nitro(N-butozycaronyl)tyrbosine-bovine serum albumin antibodies. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the membranes and hemoglobin, and subsequent Western blot analysis, showed that these antibodies only slightly bind to the bands of the proteins from both young and senescent erythrocytes, whereas these antibodies definitely bind to the protein bands of membranes and hemoglobin nitrated by NO2 or ONOOH in vitro. This result indicates that nitrotyrosine is not detected in the membrane proteins and hemoglobin in human normal erythrocytes in circulation. However, this does not conclude that erythrocytes are not exposed to reactive nitrogen species in the circulation.

The influence of sesamol, an antioxidant in processed sesame oil, on oxidative modification of human erythrocyte membrane proteins was investigated. Human erythrocytes were incubated with sesamol at various concentrations up to 10 mM at 37 degrees C for 1 h. The amounts of hemoglobin bound to the membranes and detergent C12E8-insoluble membrane protein aggregates were increased as the concentration of sesamol increased. Western blot analysis indicated that aggregates of band 3 protein were increased by the treatment. Binding of anti-band 3 antibody to the erythrocytes was increased by the treatment. Isolated cell membranes were incubated with sesamol similarly. Aggregates of band 3 protein were also increased, indicating that the band 3 protein aggregation was little affected by hemoglobin bound to the membranes. Aggregation of band 3 protein in the treatment of isolated cell membranes was partially prevented when the treatment was conducted under anaerobic conditions, suggesting that augmentation of the protein aggregation by sesamol involved both oxygen-dependent and oxygen-independent pathways. Among phenolics, sesamol showed a distinctive feature to increase band 3 protein aggregation in erythrocyte membranes and to enhance anti-band 3 binding to erythrocytes.

We have examined electrical and magnetic properties of the ${\mathrm{Sr}}_{3}$${\mathrm{V}}_{2}$${\mathrm{O}}_{7\mathrm{\ensuremath{-}}\mathit{d}}$ system. Electrical resistivity changes from metallic to semiconducting with decreasing oxygen content. Transport is governed by variable-range hopping of the elecrons since the resistivity obeys the exp(${\mathit{AT}}^{\mathrm{\ensuremath{-}}1/4}$) law at low temperature. Oxygen-deficient ${\mathrm{Sr}}_{3}$${\mathrm{V}}_{2}$${\mathrm{O}}_{7\mathrm{\ensuremath{-}}\mathit{d}}$ exhibits different temperature--magnetic susceptibility curves for zero-field-cooled and field-cooled measurements below about 15 K. We have measured also the field dependence of the magnetic susceptibility and the long-time relaxation of thermoremanent magnetization, which obeys the relationship ${\mathit{M}}_{\mathrm{TRM}}$=${\mathit{At}}^{\mathrm{\ensuremath{-}}\mathrm{\ensuremath{\alpha}}}$. The magnetic properties in the ${\mathrm{Sr}}_{3}$${\mathrm{V}}_{2}$${\mathrm{O}}_{7\mathrm{\ensuremath{-}}\mathit{d}}$ system, therefore, are interpreted to be spin-glass like caused by the localized V spins introduced by the disorder-induced localization.

Recent immunological studies demonstrated that proteins in vivo in several diseases are subjected to post-translational modification by advanced glycation end products (AGEs), suggesting a potential role of AGEs in aging and age-enhanced disease processes such as diabetic complications, atherosclerosis and Alzheimer's disease. Nvarepsilon-(Carboxymethyl)lysine (CML) is one of the major AGE-structures demonstrated in vivo so far. In the present study, membrane proteins from young erythrocyte population were compared with those from senescent erythrocytes separated from the same individual in their CML-contents using a monoclonal antibody for CML (6D12). SDS-polyacrylamide gel electrophoresis and subsequent Western blot showed that 6D12 bound to the band 1, 2, 3, 4.2, 5, 6 and 7 proteins from senescent erythrocytes, but not to those from young erythrocytes. Furthermore, quantitative estimation of the reactivity of 6D12 to these erythrocyte membranes by ELISA showed that the reactivity of 6D12 to senescent erythrocyte membranes was 3- to 6-fold higher than that of young erythrocyte membranes. These results indicate that membrane proteins of circulating erythrocytes undergo CML-modification, and the modified proteins accumulated in an age-dependent manner during the life span of erythrocytes.

Young and old human red blood cells (RBC) were separated from freshly collected human blood by Percoll density gradient centrifugation. The amounts of lipid peroxidation products in the lipid fractions of these RBC were determined by high performance liquid chromatography-chemiluminescence, thiobarbituric acid and LPO-586 methods. The levels of phosphatidylcholine and phosphatidylethanolamine hydroperoxides in old RBC were higher than in young RBC. The products reflecting the advanced stage of lipid peroxidation, malonaldehyde (free and bound forms), 4-hydroxyalkenals (free and bound forms) and other aldehydes, were also higher in old RBC than in young RBC. The levels of these lipid peroxidation products increased when whole RBC were mildly oxidized with ferric ion. These results indicate that oxidative damage of RBC in the circulation takes place during the aging process, and lipid hydroperoxides and other lipid peroxidation products accumulate in old RBC.

The aim of this study is to investigate the applicability of high-Tc-superconducting films in a fault current limiter (FCL) without liquid nitrogen (L-N2). The FCL element consists of a 200 nm-thick YBCO film having a current limiting area 4 mm wide and 90 mm long. A half-cycle-alternating voltage (50 Hz) was applied to the above element which had been cooled by a refrigerator. When a voltage of 100 Vrms (150A) was applied at 77K, the YBCO film became resistive at 13 A and the fault current rapidly decreased to 7 A in less than 0.5 ms. At lower temperature, 74K, the transition current increased to more than 30 A, while the limited current remained less than 9 A. These results suggest that a superior FCL system without L-N2 will be obtained.

The in-plane alignment of grains in YBCO superconducting films deposited on poly-crystalline Ag tapes by the ionized-cluster-beam-deposition method was investigated. All of the YBCO films obtained had c-axis orientation. It has been clarified that the in-plane alignment depends on the crystal orientation of the Ag tapes. Namely, the in-plane alignment of YBCO films was improved when Ag (110) was aligned in the tape surface. On the other hand, when the crystal orientation of the Ag tapes was random, the YBCO films did not show any alignment in the tape surface. It is considered that the growth mechanism of YBCO films is explained by the near-coincident site lattice model between YBCO and Ag lattices.

A significant enhancement of Jc in a magnetic field for Ag sheathed Bi-Pb-Sr-Ca-Cu-O (BPSCCO) tapes has been achieved by post-annealing at reduced temperature after normal processing. This post-annealing at reduced temperature introduced extra oxygen into the oxide superconductor. Weak links were eliminated and Jc has been increased in the oxygenated tapes by a factor of 1.5 to 3 at 0 T over the normally processed tapes without post-annealing. The optimized Jc values for the oxygenated tapes ranged from 30000 to 57000 A/cm2 at 77.3 K and 0 T. The irreversibility lines measured by d.c. SQUID exhibited an improvement in flux pinning in the oxygenated tapes compared with that in normally processed tapes. The introduced oxygen ions are responsible for the enhanced Jc, may work as a pinning center and affect two dimensionality in superconductivity for the BPSCCO system.

Electronic states and magnetic properties in the layered perovskite vanadium oxides Srn+1VnO3n+1 were compared to those in the high-Tc cuprate superconductors. It was revealed that the electronic states in metallic Srn+1VnO3n+1 were described as the low U metal, while the insulating Sr2VO4 had the markedly different electronic structure. In Sr2VO4 the main portion of the occupied vanadium d states was interpreted to exist below oxygen 2p states in the simplest scheme of the electronic structure. Magnetic properties of Sr2−xLax−VO4 were discussed in conjunction with the structural phase transitions.

A new layered perovskite vanadium oxide Sr4V3O8-d was synthesized and its crystal structure and magnetic properties were studied. Sr4V3O8-d has a novel crystal structure, containing a V-0 octahedron and a two-fold V-0 fence in a unit cell. It exhibits negative magnetization below 30 K. when cooled in a magnetic field. This peculiar magnetism is attributed to N-type parasitic ferrimagnetism.

A high Jc superconducting tape with Tc of 84K and Jc of 1.5×104A/cm2 at 77K, 0 T was obtained using the ICB deposition method. This tape had no buffer layer and had a high c-axis orientation of YBCO to the Ag tape surface. Increasing the acceleration voltage for the Cu cluster was found to be effective to improve the surface smoothness of the YBCO film. The cross-sectional view of a high-resolution transmission micrograph showed no amorphous layer or precipitates in the boundary between the YBCO film and the Ag substrate.

The relation between the carrier concentration and the transition temperature was examined in the modulation-free Bi 2212 high TC superconductor. Modulation-free Bi2−xPbxSr2Cal−yYyCu2O8+d samples were prepared with appropriate values of x and y, which gave no extra oxygen in the Bi-O layer. Tc showed the initial increase and decreased with increasing Y concentration. At the same time, the volume fraction of the superconductivity decreased rapidly. These changes in the superconducting properties are in the same manner as in Bi2Sr2Cal−yYyCu2O8+d samples, but the temperature range in which the Tc changes occurred was higher in the modulation free, Pb-substituted samples. Thus, the carrier concentration change by Ca/Y replacement and the Tc increase derived by Bi/Pb replacement are considered to occur independently. These results indicate that the increase in Tc by Bi/Pb substitution is not attributed to the change in the carrier concentration, but to the relaxation of the structure modulation itself.

Changes in magnetic properties by Fe or Zn substitution in Pb2Sr2Ca0.25Y0.75Cu3-xTMxO8 superconductor and in related antiferromagnetic insulator Pb2Sr2YCu3-xTMxO8 were examined. Superconductivity was reduced with increasing Fe or Zn content, and Curie paramagnetism was observed. Apparent magnetic moment J per one Zn atom in Pb2Sr2Ca0.25Y0.75Cu2.86Zn0.14O8 was 0.33 Pb2Sr2YCu2.9Zn0.1O8 substituted Zn in AFI shows Curie paramagnetic character. Apparent J=0.4 for Pb2Sr2YCu2.9Zn0.1O8 was derived. 0.66 Cu spins for Pb2Sr2Ca0.25Y0.75Cu2.86Zn0.14O8 or 0.8 Cu spins for Pb2Sr2YCu2.9Zn0.1O8 surrounding non-magnetic Zn2+ show paramagnetic character. Considering these results, disappearance of superconductivity by Fe or Zn dopig is attributed to destruction of fluctuated antiferromagnetically ordered Cu spins, which agrees with model in which localized Cu spins and antiferromagnetic order exist, even in the superconducting state.

We have investigated the relationship between microstructure and pinning forces. The boundaries between grains a-axis oriented and c-axis oriented are clarified to be effective as a pinning center.