ABSTRACT
We report an experimental study of the bimagnetic nanocomposites CoFe2/CoFe2O4. The precursor material, CoFe2O4 was prepared using the conventional stoichiometric combustion method. The nano-structured material CoFe2/CoFe2O4 was obtained by total oxygen reduction of CoFe2O4 using a thermal treatment at 350 °C in H2 atmospheres following the partial oxidation in O2 atmospheres at 380 °C during 120; 30; 15, 10, and 5 min. The X-ray diffraction, Mössbauer spectroscopy and transmission electronic microscopy images confirmed the formation of the material CoFe2/CoFe2O4. The magnetic hysteresis for the nanocomposite with different saturation magnetization (from 87 to 108 emu/g) also confirms the formation of the CoFe2/CoFe2O4 with different content of CoFe2O4. Furthermore, the magnetic hysteresis curves for all samples presented a single magnetic behavior, suggesting the magnetic coupling between the phases of the nanocomposite. The effects of high energy milling on the magnetic properties of the precursor material and nanocomposites samples were evaluated.
Subject(s)
Cobalt , Nanocomposites , Ferric Compounds , MagneticsABSTRACT
BACKGROUND AND PURPOSE: Previous in vitro and in vivo studies of the effects of nitric oxide synthase inhibition in the central nervous system have yielded conflicting results concerning the role of nitric oxide in the events that lead to ischemic injury. In this study, we tested the hypothesis that preischemic inhibition of nitric oxide synthase increases infarct volume after reversible focal cerebral ischemia in rats. METHODS: NG-nitro-L-arginine methyl ester hydrochloride 15 mg/kg IV or an equivalent volume of saline was administered to adult Wistar rats 15 minutes before middle cerebral artery occlusion by the intraluminal suture method. After 2 hours of ischemia, the suture was withdrawn, and rats were allowed to survive for 3 days. Areas of infarction in 10 hematoxylin-eosin-stained sections were measured and used to determine infarct volume. RESULTS: Administration of NG-nitro-L-arginine methyl ester hydrochloride increased hemispheric infarct volume by 137% over control (60.9 +/- 30.5 to 144.3 +/- 19.6 mm3, P < .05; mean +/- SEM). Cortical and subcortical infarct volumes were increased by 176% (33.8 +/- 21.9 to 93.3 +/- 15.2 mm3, P < .05) and 103% (25.1 +/- 9.4 to 51.0 +/- 5.5 mm3, P < .03), respectively. CONCLUSIONS: Nitric oxide synthase inhibition increases infarct volume and decreases the variability of the response to middle cerebral artery occlusion in Wistar rats, a strain that is normally resistant to focal cerebral ischemic injury owing to extensive collateralization. The mechanism of the deleterious effect of nitric oxide synthase inhibition likely involves a more severe degree of blood flow reduction during and after middle cerebral artery occlusion, primarily by preventing the vasodilatory response of collateral vessels to proximal middle cerebral artery occlusion. Maintenance of nitric oxide synthase activity during and after focal cerebral ischemia appears to minimize ischemic injury.