Redox characteristics variations in the cation-ordered perovskite oxides BaLnMn2O5+δ (Ln = Y, Gd, Nd, and La) and Ca2Al1-xGaxMnO5+δ (0 ≤x≤ 1).

Two series of manganese-based oxygen storage materials, BaLnMn(2)O(5+δ) (Ln = Y, Gd, Nd, and La) and Ca(2)Al(1-x)GaxMnO(5+δ) (0 ≤x≤ 1), were synthesized and characterized to clarify cationic substitution effects on the oxygen intake/release behaviors of these materials. The thermogravimetric data revealed that the isovalent substitutions neighboring the active sites for oxygen intake/release are very effective. For BaLnMn(2)O(5+δ), fully-reduced δ≈ 0 products with larger Ln ions showed oxygen intake starting at lower temperatures in flowing O(2) gas, resulting in a systematic relationship between the onset temperature and the ionic radius of Ln(3+). Furthermore, the δ vs. P(O(2)) plots at 700 °C indicated a systematic trend: the larger the ionic size of Ln(3+) is, the larger oxygen contents the Ln-products exhibit. For Ca(2)Al(1-x)GaxMnO(5+δ), on the other hand, the temperature-induced oxygen intake/release characteristics appeared to be influenced by Ga-for-Al substitution, where the onset temperatures of oxygen release (upon heating) and oxygen intake (upon cooling) are decreased with the increasing Ga content (x).

Multiferroic grain boundaries in oxygen-deficient ferroelectric lead titanate.

Ultimately thin multiferroics arouse remarkable interest, motivated by the diverse utility of coexisting ferroelectric and (anti)ferromagnetic order parameters for novel functional device paradigms. However, the ferroic order is inevitably destroyed below a critical size of several nanometers. Here, we demonstrate a new path toward realization of atomically thin multiferroic monolayers while resolving a controversial origin for unexpected "dilute ferromagnetism" emerged in nanocrystals of nonmagnetic ferroelectrics PbTiO3. The state-of-the-art hybrid functional of Hartree-Fock and density functional theories successfully identifies the origin and underlying physics; oxygen vacancies interacting with grain boundaries (GBs) bring about (anti)ferromagnetism with localized spin moments at the neighboring Ti atoms. This is due to spin-polarized defect states with broken orbital symmetries at GBs. In addition, the energetics of oxygen vacancies indicates their self-assembling nature at GBs resulting in considerably high concentration, which convert the oxygen-deficient GBs into multiferroic monolayers due to their atomically thin interfacial structure. This synthetic concept that realizes multiferroic and multifunctional oxides in a monolayered geometry through the self-assembly of atomic defects and grain boundary engineering opens a new avenue for promising paradigms of novel functional devices.

Up-regulation of interleukin-2 mRNA in children with idiopathic nephrotic syndrome.

The current hypothesis for the pathogenesis of childhood idiopathic nephrotic syndrome (INS) favors the involvement of a T cell-mediated immune response. Various cytokines derived from T cells may play a critical role in INS. Previous studies have measured serum or urine cytokine levels and suggest an imbalance of the T cell-mediated immune response. To elucidate the true profile of T cell-derived cytokines, we determined interleukin (IL)-2, interferon (IFN)-gamma, IL-4, IL-10, and tumor necrosis factor (TNF)-alpha mRNA expression in children with INS. We collected mRNA from peripheral blood mononuclear cells together with plasma and urine from nine children in the acute and remission phases of INS. Expression of IL-2, IFN-gamma, IL-4, IL-10, and TNF-alpha mRNA was determined by a quantitative real-time PCR assay. Plasma and urine cytokine concentrations were measured using a specific enzyme-linked immunosorbent assay. These data were compared between the acute and remission phase in the same patients. The IL-2 mRNA levels were significantly higher in the acute phase than in the remission phase, whilst no significant difference was found in the other cytokines investigated. There was no significant difference in the plasma and urine cytokine concentrations between the acute and remission phase. Our results indicate increased expression of IL-2 mRNA in the acute phase of INS, suggesting that IL-2, at least in part, might be involved in the pathophysiology of childhood INS.

Analysis of glomerular anionic charge status in children with IgA nephropathy using confocal laser scanning microscopy.

BACKGROUND: The proteinuria resulting from IgA nephropathy is secondary to altered charge-selective and/or size-selective properties of the glomerular capillary walls. However, the functional changes occurring within the glomerular capillary network which lead to proteinuria are still poorly understood. In this study, we analyzed the participation of charged components in the glomerular capillary and their role with respect to proteinuria in childhood IgA nephropathy. METHODS: We examined glomerular anionic charge in renal biopsy specimens with confocal laser scanning microscopy using FITC-conjugated poly-L-lysine as a cationic tracer. The renal specimens investigated were from 9 children with IgA nephropathy (IgAN(+)) associated with detectable proteinuria in a morning urine specimen, 8 children with IgA nephropathy (IgAN(-)) and 11 children with thin basement membrane disease (TBMD) with no detectable proteinuria. RESULTS: The labeling intensity of glomerular fixed anionic sites from IgAN(+) was significantly lower than that of IgAN(-) and TBMD. Staining the serial sections following methylation treatment revealed that the labeling intensity for fixed anionic sites in TBMD was significantly higher than that of both IgAN(+) and IgAN(-). On the other hand, saponification treatment resulted in significantly more intensive fluorescence in TBMD and IgAN(-) than in IgAN(+). Furthermore, statistical analysis demonstrated a significant correlation between 24-hour protein excretion and the intensity of fixed anionic sites in all patients with IgA nephropathy at pH 7.0 and following staining with saponification treatment. CONCLUSIONS: These findings suggest that a reduction of glomerular anionic charge might be causally associated with the development of proteinuria in childhood IgA nephropathy. Furthermore, sulfate components such as heparan sulfate proteoglycan might be involved initially followed by carboxyl components such as sialoglycoproteins in the glomeruli of patients with IgA nephropathy contributing to the occurrence of proteinuria. We suggest that this method represents a straightforward approach to dissect the participation of charged components in the pathogenesis of childhood IgA nephropathy and their relationship to the development of glomerular proteinuria.

Quantitative analysis of glomerular type IV collagen alpha3-5 chain expression in children with thin basement membrane disease.

Thin basement membrane disease (TBMD) and Alport syndrome, two forms of childhood nephritis, have generally been considered to be hereditary diseases. In Alport syndrome, several reports have demonstrated pathogenic mutations of the genes encoding type IV collagen alpha3, 4 and/or 5 chain [alpha3, 4 and/or 5(IV)]. Previous immunohistochemical studies indicated that these antigens were absent from the glomerular basement membrane (GBM) in Alport syndrome, whilst a normal labeling pattern was maintained in TBMD. In order to understand the role of the alpha3, 4 and/or 5(IV) antigens in TBMD, we used confocal laser scanning microscopy (CLSM) to examine cryosections of renal biopsies from 12 children with TBMD and 11 control children with IgA nephropathy (IgAN) without proteinuria. All tissue sections were stained with a mixture of FITC-conjugated rat monoclonal antibodies directed against human alpha3(IV), alpha4(IV) or alpha5(IV) and a Texas red-conjugated rat monoclonal antibody raised against human alpha2(IV). CLSM was performed and quantitative analysis of the ratio of the staining signal for alpha3(IV), alpha4(IV) or alpha5(IV) to alpha2(IV) [alpha3(IV), alpha4(IV) or alpha5(IV)/alpha2(IV)] along the GBM was determined. The average number of pixels for alpha3(IV), alpha4(IV) or alpha5(IV)/alpha2(IV) was 3.52 +/- 1.49, 3.54 +/- 1.25 and 1.09 +/- 0.49 in TBMD and 3.62 +/- 1.46, 3.99 +/- 1.53 and 1.77 +/- 0.47 in control subjects, respectively. Statistical analysis indicated that alpha5(IV)/alpha2(IV) ratio was significantly lower (p < 0.01) in children with TBMD compared to controls. These findings raise the possibility that TBMD might be caused by an abnormality of the alpha5(IV) antigen along the GBM.

[Shear stress-induced platelet aggregation in children with minimal change nephrotic syndrome].

Analysis of the hemostasis system using biochemical techniques in children with minimal change nephrotic syndrome (MCNS) has previously been restricted to in vitro assays. The recent introduction of measurement of shear stress-induced platelet aggregation (SIPA) using platelet-rich plasma (PRP) has facilitated detailed investigation of the hemostatic system in vivo. In order to further analyze the etiology of the thrombotic tendency exhibited by patients with childhood MCNS, we investigated SIPA at both low shear stress (L-SIPA) and high shear stress (H-SIPA) in 14 children with MCNS using PRP collected weekly after commencing prednisolone therapy. Seven patients were newly diagnosed cases of MCNS (ND) whereas the remainder had suffered a disease relapse (DR). Prior to prednisolone therapy L-SIPA, which was thought to be affected by fibrinogen (Fbg) levels, was significantly increased in both patient groups compared to normal controls (17.4 +/- 4.1% vs. 3.6 +/- 0.7%, ND vs control, p < 0.01: 11.7 +/- 3% vs. 2 +/- 0.7%, DR vs control, p < 0.01) with values declining at weekly intervals thereafter. Plasma Fbg levels in simultaneously collected samples followed a similar course. In contrast, H-SIPA, which was thought to be affected by von Willebrand factor (VWF), was significantly enhanced in MCNS patients after 1 week of prednisolone therapy compared to the controls (45 +/- 5.1% vs. 26.3 +/- 3.5%, ND vs normal, p < 0.05: 36.9 +/- 3.3% vs. 25.5 +/- 1.6%, DR vs. normal, p < 0.05). Plasma ristocetin cofactor and VWF antigen levels in simultaneously collected samples followed a similar course, whereas thrombin-antithrombin complex (TAT) levels remained constant. These results indicate that SIPA is enhanced in the acute stage of childhood MCNS, especially L-SIPA prior to the initiation of prednisolone therapy and H-SIPA after 1 week of prednisolone therapy, and that these phenomena may be affected by plasma Fbg and VWF levels, respectively. The enhanced SIPA may play an important thrombogenic role in the acute phase of childhood MCNS.