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- Esir, S., et al.
(författare)
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SrFe12O19/Zn0.65Ni0.25Cu0.1Fe2O4 Core-Shell Nanocomposite : Synthesis, Chracterization and Catalytic Activity in Aqueous Solution
- 2014
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Ingår i: Journal of inorganic and organometallic polymers and materials. - : Springer Science and Business Media LLC. - 1574-1443 .- 1574-1451. ; 24:4, s. 722-728
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Tidskriftsartikel (refereegranskat)abstract
- SrFe12O19/Zn0.65Ni0.25Cu0.1Fe2O4 core-shell nanocomposite has been successfully synthesized by sol-gel autocombustion (for SrFe12O19, core) and hydrothermal methods (for Zn0.65Ni0.25Cu0.1Fe2O4, shell). The products were characterized by X-ray powder diffractometer, transmission electron microscopy, fourier transform infrared spectrsocopy, vibrating sample magnetometer, Ultraviolet-visible specroscopy and inductively coupled plasma. Both X-ray powder diffraction, transmission electron microscopy results showed that Zn0.65Ni0.25Cu0.1Fe2O4 shell is on the surface of the SrFe12O19 core. The variations between the magnetic properties of the precursors and nanocomposite may be explained by interphase interactions at the surface of two ferrites. The properties of the SrFe12O19/Zn0.65Ni0.25Cu0.1Fe2O4 core-shell nanocomposite were favourable in its separation, recycling and reuse after reaction. The catalytic activity of SrFe12O19/Zn0.65Ni0.25Cu0.1Fe2O4 core-shell nanocomposite in the presence of NaBH4 were tested against methyl violet.
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- Konradsson-Geuken, A, et al.
(författare)
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Cortical kynurenic acid bi-directionally modulates prefrontal glutamate levels as assessed by microdialysis and rapid electrochemistry.
- 2010
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Ingår i: Neuroscience. - : Elsevier BV. - 0306-4522 .- 1873-7544. ; 169:4
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Tidskriftsartikel (refereegranskat)abstract
- Using two in vivo methods, microdialysis and rapid in situ electrochemistry, this study examined the modulation of extracellular glutamate levels by endogenously produced kynurenic acid (KYNA) in the prefrontal cortex (PFC) of awake rats. Measured by microdialysis, i.p. administration of KYNA's bioprecursor L-kynurenine dose-dependently elevated extracellular KYNA and reduced extracellular glutamate (nadir after 50 mg/kg kynurenine: 60% decrease from baseline values). This dose-dependent decrease in glutamate levels was also seen using a glutamate-sensitive microelectrode array (MEA) (31% decrease following 50 mg/kg kynurenine). The kynurenine-induced reduction in glutamate was blocked (microdialysis) or attenuated (MEA) by co-administration of galantamine (3 mg/kg i.p.), a drug that competes with KYNA at an allosteric potentiating site of the alpha 7 nicotinic acetylcholine receptor. In separate experiments, extracellular glutamate levels were measured by MEA following the local perfusion (45 min) of the PFC with kynurenine (2.5 microM) or the selective KYNA biosynthesis inhibitor S-ethylsulfonylbenzoylalanine (S-ESBA; 5 mM). In agreement with previous microdialysis studies, local kynurenine application produced a reversible reduction in glutamate (nadir: -29%), whereas perfusion with S-ESBA increased glutamate levels reversibly (maximum: +38%). Collectively, these results demonstrate that fluctuations in the biosynthesis of KYNA in the PFC bi-directionally modulate extracellular glutamate levels, and that qualitatively very similar data are obtained by microdialysis and MEA. Since KYNA levels are elevated in the PFC of individuals with schizophrenia, and since prefrontal glutamatergic and nicotinic transmission mediate cognitive flexibility, normalization of KYNA levels in the PFC may constitute an effective treatment strategy for alleviating cognitive deficits in schizophrenia.
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