Structural Coloration of a Colloidal Amorphous Array is Intensified by Carbon Nanolayers

In this study, we introduce the possibility of applying a colloidal amorphous array composed of fine silica particles as a structural-color material to invisible information technology. The appearance of a thick filmlike colloidal amorphous array formed from fine silica particles is considerably influenced by incoherent light scattering across the entire visible region. Therefore, regardless of the diameter of the fine silica particles, the thick colloidal amorphous array exhibits a white color to the naked eye. When carbon is uniformly deposited in the colloidal amorphous array by a pressure-pulsed chemical vapor deposition method, incoherent light scattering in the colloidal amorphous array is suppressed. As a result, coherent light scattering due to the short-range order in the colloidal amorphous array becomes conspicuous and the array exhibits a vivid structural color. As structures, such as letters and pictures, can be drawn using this technology, the colloidal amorphous array as a structural-colored material may also be applicable for invisible information technology

Systemic Manifestations in Pyridox(am)ine 5'-Phosphate Oxidase Deficiency.

Abstract Objective Pyridoxine is converted to its biologically active form pyridoxal-5-phosphate (P5P) by the enzyme pyridox(am)ine 5′-phosphate oxidase and serves as a cofactor in nearly 200 reactions in the central nervous system. Pyridox(am)ine 5′-phosphate oxidase deficiency leads to P5P dependent epilepsy, typically a neonatal- or infantile-onset epileptic encephalopathy treatable with P5P or in some cases, pyridoxine. Following identification of retinopathy in a patient with pyridox(am)ine 5′-phosphate oxidase deficiency that was reversible with P5P therapy, we describe the systemic manifestations of pyridox(am)ine 5′-phosphate oxidase deficiency. Methods A series of six patients with homozygous mutations of PNPO , the gene coding pyridox(am)ine 5′-phosphate oxidase, were evaluated in our center over the course of two years for phenotyping of neurological and systemic manifestations. Results Five of six were born prematurely, three had anemia and failure to thrive, and two had elevated alkaline phosphatase. A movement disorder was observed in two children, and a reversible retinopathy was observed in the most severely affected infant. All patients had neonatal-onset epilepsy and were on a continuum of developmental delay to profound encephalopathy. Electroencephalographic features included background slowing and disorganization, absent sleep features, and multifocal and generalized epileptiform discharges. All the affected probands carried a homozygous PNPO mutation (c.674 G>T, c.686 G>A and c.352G>A). Conclusion In addition to the well-described epileptic encephalopathy, pyridox(am)ine 5′-phosphate oxidase deficiency causes a range of neurological and systemic manifestations. A movement disorder, developmental delay, and encephalopathy, as well as retinopathy, anemia, and failure to thrive add to the broadening clinical spectrum of P5P dependent epilepsy

Experience With Lacosamide in a Series of Children With Drug-Resistant Focal Epilepsy

We report our pediatric experience with lacosarnide, a new antiepileptic drug, approved by the US Food and Drug Administration as adjunctive therapy in focal epilepsy in patients more than 17 years old. We retrospectively reviewed charts for lacosamide use and seizure frequency outcome in patients with focal epilepsy (Wilcoxon signed rank test). Sixteen patients (7 boys) were identified (median dose 275 mg daily, 4.7 mg/kg daily; mean age 14.9 years, range 8-21 years). Patients were receiving a median of 2 antiepileptic drugs (interquartile range [IQR] 1.7-3) in addition to having undergone previous epilepsy surgery (n = 3), vagus nerve stimulation (n = 9), and ketogenic diet (n = 3). Causes included structural (encephalomalacia and diffuse encephalitis, 1 each; stroke in 2) and genetic abnormalities (Aarskog and Rett syndromes, 1 each) or cause not known (n = 10). Median seizure frequency at baseline was 57 per month (IQR 7-75), and after a median follow-up of 4 months (range 1-13 months) of receiving lacosamide, it was 12.5 per month (IQR 3-75), (P < 0.01). Six patients (37.5%; 3 seizure free) were classified as having disease that responded to therapy (>= 50% reduction seizure frequency) and 10 as having disease that did not respond to therapy (<50% in 3; increase in 1; unchanged in 6). Adverse events (tics, behavioral disturbance, seizure worsening, and depression with suicidal ideation in 1 patient each) prompted lacosamide discontinuation in 4/16 (25%). This retrospective study of 16 children with drug-resistant focal epilepsy demonstrated good response to adjunctive lacosamide therapy (median seizure reduction of 39.6%; 37.5% with >= 50% seizure reduction) without severe adverse events. (C) 2011 Elsevier Inc. All rights reserved.Brazilian government[4225-09-0