RESUMO
In the present work, we report on the synthesis of peptide functionalized magneto-plasmonic nanoparticles in a simple microfluidic platform. Superparamagnetic nanoparticles and gold nanorods were selected for this study. Magnetic nanoparticles were functionalized with peptide D1, which can bind selectively to toxic aggregates of the ß-amyloid peptide associated with Alzheimer's disease. Gold nanorods were functionalized with chitosan replacing the surfactant cetyltrimethylammonium bromide to reduce the cytotoxic effect. The selected microfluidic strategy yields structures with plasmonic and magnetic properties in a nanostructure. Cytotoxic assays with SH-SY5Y cells demonstrate that nanoparticles obtained by microfluidics do not affect cell viability at the studied concentrations. Additionally, these magneto-plasmonic nanoparticles inhibit fibril formation demonstrating that the magneto-plasmonic nanoparticles obtained by microfluidics could be applied for a potential treatment and diagnosis of Alzheimer's disease.
RESUMO
1. Crude synaptosomes (P2) and synaptosomal membranes were prepared from normal C57/B110 mouse brains and Wistar rats respectively. 2. [3H]Pro binding to mouse brain synaptic membranes was examined in the presence of competitive NMDA antagonist, MK-801, or HA-966. Conversely, the effects of l-proline on [3H]MK-801 binding were also probed. The effects of l-proline on glutamate-medicated [Ca+2]i levels were tested. 3. The authors could not detect any effect of proline on glutamate-mediated [CA+2]i levels using FURA-2 in synaptosomes or neuroblastoma cells. 4. NMDA competitive antagonists, AP-7, CPP, and CGS 19755 inhibit [3H]Pro binding to mouse brain synaptic membranes. 5. MK-801, a NMDA channel blocker, also inhibits [3H]Pro binding, but 200 mM proline is incapable of inhibiting [3H]MK-801 binding. 6. HA-966, a glycine site partial agonist inhibits [3H]Pro binding. Proline has modest effects on [3H]glycine binding.
Assuntos
Sistema Nervoso Central/efeitos dos fármacos , Interações Medicamentosas , Ácido Glutâmico/farmacologia , Prolina/farmacologia , Animais , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Ratos , Ratos WistarAssuntos
Eletroencefalografia , Epilepsia/fisiopatologia , Ácido Glutâmico/metabolismo , Convulsões/fisiopatologia , Transmissão Sináptica/fisiologia , Estimulação Acústica , Fatores Etários , Animais , Encéfalo/patologia , Encéfalo/fisiopatologia , Mapeamento Encefálico , Técnicas de Cultura , Epilepsia/genética , Epilepsia/patologia , Feminino , Genótipo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Convulsões/genética , Convulsões/patologia , Sinaptossomos/patologia , Sinaptossomos/fisiologiaRESUMO
The prevalence of epilepsy among children born in 1966 and reaching the age of 9 years during 1975 was investigated in Melipilla, Chile, using questions similar to those used by Rose et al. (1973). Of 2,104 potential respondents, 2,085 were interviewed. A sample of 593 children received neurological examination and 455 received an electroencephalogram. The prevalence rates for epilepsy were higher than those reported in two American studies using the same methodology. The possibility of socioeconomic factors to account for these differences was considered. Prevalence rates for simple febrile convulsions and minimal brain dysfunction were similarly calculated.