Noble microfluidic system for bioceramic nanoparticles engineering.

Bioceramic nanoparticles have many potential applications within the biomedical device industry. However, these applications demand a precise control of their sizes, shapes and morphology which play a main role in most properties. In this work, we report a new route for the synthesis of hydroxyapatite nanoparticles using a microfluidic device. The process is carried out by continuous laminar flow through the device. The obtained nanoparticles have showed same properties (composition, length, orientation, roughness) than those produced by conventional methods, however, our device can afford to fine tune the structure via simple engineering, i.e., produce nanoparticles of different size only by varying the flow velocity. In addition to the efficiency and novelty of this system, the optimization of personnel costs makes it very profitable economically.

Peptide functionalized magneto-plasmonic nanoparticles obtained by microfluidics for inhibition of ß-amyloid aggregation.

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.

Altered GABAergic and glutamatergic transmission in audiogenic seizure-susceptible mice.

The C57BL/10 SPS/sps mouse mutant are audiogenic seizure-susceptible. The enzymatic activities of glutamate decarboxylase (GAD), GABA aminotransferase (GABA-T), alanine aminotransferase (ALA-T), aspartate aminotransferase (ASP-T), and glutamate dehydrogenase (GDH) of whole brain supernatant are significantly reduced in these epileptic mice. GABA uptake is decreased in cortex, midbrain, and pons medulla. Previous studies showed the presence of two sodium-dependent GLU uptake systems in normal (SPS/SP) mice. Glutamate Umax by System 1 is significantly decreased in these mice, whereas the Umax value for System 2 is significantly increased in the epileptic mice.

Inhibition of high-affinity [3H]L-proline binding to rat brain membranes by 2-amino-7-phosphonoheptanoic acid.

L-Glutamate and 2-amino-7-phosphonoheptanoic acid [corrected] (AP-7) (10(-9) to 10(-6) M), a competitive NMDA (N-methyl-D-aspartate) antagonist, inhibit approximately 60% of [3H]L-proline binding to rat membranes from midbrain. In hippocampal membranes, AP-7 inhibits proline binding by 80%, while in cerebellar membranes AP-7 had little effect. These results are indicative of the possible neuromodulatory role of proline in the central nervous system, possibly through the NMDA receptor(s).

High affinity [3H]glutamate uptake systems in normal and audiogenic seizure-susceptible mice.

Two high affinity sodium-dependent and PDC-sensitive glutamate (GLU) uptake systems are present in a whole brain synaptosomal preparation from adult C57BL/10 SPS/SPS normal mice. System 1 has an apparent Km of 3.65 microM while that of System 2 is 46.8 microM. Glutamate uptake in the normal mice increases gradually during development, displaying a striking peak at postnatal day 15, and decreases rapidly between PN 16 and PN 20 until it reaches adult levels. The developmental pattern of GLU uptake System 1 and System 2 in audiogenic seizure susceptible mice is similar to that described in normal mice. However, there are differences between GLU uptake system 1 and 2 during ontogenesis: (1) System 1 could not be detected until PN 15 while being markedly diminished in adulthood; and (2) GLU uptake by System 2 is increased in adults. In addition, the Umax for System 2 is significantly greater than that of normal mice at PN 2 and PN 15.

Proline-glutamate interactions in the CNS.

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.

Possible regulation of high-affinity glutamate uptake in synaptosomes of normal and epileptic mice.

Glutamate (Glu) uptake is the primary mechanism for its removal from the synapse. In genetic audiogenic seizures (AGS), Glu uptake is elevated prior to the appearance of seizures. Increased Glu uptake is also observed in synaptosomes from normal mice preincubated with lithium or nitroarginine, an NO synthase inhibitor. Pertussis and cholera toxins cause a marked reduction in Glu uptake. In contrast, neither lithium nor nitroarginine affected Glu uptake by synaptosomes from genetic epileptic mice. Arachidonic acid inhibits Glu uptake, whereas synaptosomes from epileptic mouse brain appear to be more sensitive to arachidonic acid as indicated by a shift of the inhibition curve to the left. These observations are indicative of the possible regulation of Glu uptake by second messengers and its alteration in genetic epilepsy.

Prevalence of epilepsy in children of Melipilla, Chile.

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.

GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of absence seizures.

The C57BL/10 sps/sps mouse mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps/sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca(2+)-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL/10 sps/sps mice.