Neutron reflectometry studies of Gd/Nb and Cu30Ni70/Nb superlattices

We performed a comparative study of magnetic proximity effects in [Gd(5nm)/Nb(25nm)]12 and [Cu30Ni70(6nm)/Nb(27nm)]12 superlattices of S/F type by means of transport measurements and neutron scattering. Transport measurements have shown that Gd/Nb and CuNi/Nb superlattices shows 3D and 2D type of superconductivity respectively. In the case of proximity coupled Gd/Nb superconductor the effective thickness of the superconducting region, 300nm is enough to expel significant amount of applied magnetic field which was detected by neutron scattering. In decoupled CuNi/Nb superlattice thickness of every superconducting layer is only 27nm which is not enough to expel applied magnetic field. Our study shows how neutron reflectometry can be applied to study proximity coupling in superconducting/ferromagnet heterostructures

High-Fat Diet Induces Apoptosis of Hypothalamic Neurons

Consumption of dietary fats is amongst the most important environmental factors leading to obesity. In rodents, the consumption of fat-rich diets blunts leptin and insulin anorexigenic signaling in the hypothalamus by a mechanism dependent on the in situ activation of inflammation. Since inflammatory signal transduction can lead to the activation of apoptotic signaling pathways, we evaluated the effect of high-fat feeding on the induction of apoptosis of hypothalamic cells. Here, we show that consumption of dietary fats induce apoptosis of neurons and a reduction of synaptic inputs in the arcuate nucleus and lateral hypothalamus. This effect is dependent upon diet composition, and not on caloric intake, since pair-feeding is not sufficient to reduce the expression of apoptotic markers. The presence of an intact TLR4 receptor, protects cells from further apoptotic signals. In diet-induced inflammation of the hypothalamus, TLR4 exerts a dual function, on one side activating pro-inflammatory pathways that play a central role in the development of resistance to leptin and insulin, and on the other side restraining further damage by controlling the apoptotic activity

Chirality of Bloch domain walls in exchange-biased CoO/Co bilayer studied by waveguide-enhanced neutron spin-flip scattering

Magnetic state of exchanged biased CoO(20nm)/Co($d_F$) bilayer ($d_F$=5-20nm) was studied by means of polarized neutron reflectometry. By spacing of CoO/Co bilayer and Al$_2$O$_3$ substrate with Nb(20nm) layer we created waveguide structure which allowed us to significantly enhance intensity of spin-flip (SF) scattering in the position of optical resonances. For the trained sample with thinnest Co(5nm) we detected strong SF scattering at the resonance position (up to 30\% of incoming intensity) speaking about high non-collinearity of the system. As $d_F$ increases, the intensity of SF scattering linearly decreases. At the same time we observed asymmetry of up-down and down-up scattering channels at the resonance positions. We attribute this asymmetry to the Zeeman splitting of neutrons energies with different initial polarization taking place in high external field. Analysis, however, shows that the applied in the PNR experiment external field is not enough to quantitatively explain the observed asymmetry for the samples with $d_F >$ 5nm and we have to postulate presence of additional magnetic field produced by sample. We attribute this additional field to the stray field produced by chiral Bloch domain walls. The chirality of the domain walls can be explained by Dzyaloshinskii-Moriya interaction arising at the CoO/Co interface. Our results can be useful for designing of spintronic devices using exchange bias effect

Evolution of non-collinear magnetic state of exchange biased ferromagnet/normal metal/ferromagnet/superconductor heterostructure in magnetic field studied by polarized neutron reflectometry

By using waveguide enhanced polarized neutron reflectometry we have characterized the magnetic state of exchange biased CoO x(20 nm)/Co(4 nm)/Nb(5 nm)/Co(2 nm)/Nb(25 nm)/Al₂O₃ system. Measurement allowed to determine the dependence of the inclination angles of magnetic moment of the both Co layers as a function of applied field. According to the measurement the soft Co(2 nm) layer magnetization turns towards external field in magnetic fields as small as 20 Oe. In contrast direction of magnetic moment of Co(4 nm) layer cannot be altered in magnetic fields as high as 2 kOe

The role of proliferator-activated receptor γ coactivator–1α in the fatty-acid–dependent transcriptional control of interleukin-10 in hepatic cells of rodents

Interleukin-10 (IL-10) is an endogenous factor that restrains hepatic insulin resistance in diet-induced steatosis. Reducing IL-10 expression increases proinflammatory activity in the steatotic liver and worsens insulin resistance. As the transcriptional coactivator proliferator-activated receptor γ coactivator–1 α (PGC-1 α) plays a central role in dysfunctional hepatocytic activity in diet-induced steatosis, we hypothesized that at least part of the action of PGC-1 α could be mediated by reducing the transcription of the IL-10 gene. Here, we used immunoblotting, real-time polymerase chain reaction, immunocytochemistry, and chromatin immunoprecipitation assay to investigate the role of PGC-1 α in the control of IL-10 expression in hepatic cells. First, we show that, in the intact steatotic liver, the expressions of IL-10 and PGC-1 α are increased. Inhibiting PGC-1 α expression by antisense oligonucleotide increases IL-10 expression and reduces the steatotic phenotype. In cultured hepatocytes, the treatment with saturated and unsaturated fatty acids increased IL-10 expression. This was accompanied by increased association of PGC-1 α with c-Maf and p50–nuclear factor (NF) κB, 2 transcription factors known to modulate IL-10 expression. In addition, after fatty acid treatment, PGC-1 α, c-Maf, and p50-NF κB migrate from the cytosol to the nuclei of hepatocytes and bind to the IL-10 promoter region. Inhibiting NF κB activation with salicylate reduces IL-10 expression and the association of PGC-1 α with p50-NF κB. Thus, PGC-1 α emerges as a potential transcriptional regulator of the inflammatory phenomenon taking place in the steatotic liver592215223CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPNão temNão te

Taurine enhances the anorexigenic effects of insulin in the hypothalamus of rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Taurine is known to modulate a number of metabolic parameters such as insulin secretion and action and blood cholesterol levels. Recent data have suggested that taurine can also reduce body adiposity in and in rodents. Since body adiposity is mostly regulated by insulin-responsive hypothalamic neurons involved in the control of feeding and thermogenesis, we hypothesized that some of the activity of taurine in the control of body fat would be exerted through a direct action in the hypothalamus. Here, we show that the intracerebroventricular injection of an acute dose of taurine reduces food intake and locomotor activity, and activates signal transduction through the Akt/FOXO1, JAK2/STAT3 and mTOR/AMPK/ACC signaling pathways. These effects are accompanied by the modulation of expression of NPY. In addition, taurine can enhance the anorexigenic action of insulin. Thus, the aminoacid, taurine, exerts a potent anorexigenic action in the hypothalamus and enhances the effect of insulin on the control of food intake.42624032410Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq