25 research outputs found
P-07: Vascular Anomalies Associated With Esophageal Atresia and Tracheoesophageal Fistula: Incidence, Clinical Presentation, Diagnosis and Consequences.
Synthesis of SiO2-coated Bi2S3/ poly(styrene) nanocomposites by in-situ polymerization
New nanocomposites containing silica-coated Bi2S3 nanofibers were synthesised by in situ polymerization using two distinct synthetic strategies: emulsion and suspension polymerization. Transmission and scanning electron microscopy of the nanocomposite particles showed that in both cases the Bi2S3/SiO2 nanoparticles were densely coated with poly(styrene). In situ emulsion polymerization afforded nanocomposites in which the nanofibers were coated with polymer spheres whilst suspension polymerization gives rise to a homogeneous polymer layer coat. The morphology of the poly(styrene) coating observed is discussed considering the surface modification of the nanofibers and the polymerization technique involved
Cerebellar leukoencephalopathy: most likely histiocytosis-related
Background: Histiocytosis, both Langerhans and non-Langerhans cell type, can be associated with cerebellar white matter abnormalities, thought to be paraneoplastic. The associated clinical picture consists of ataxia, spasticity, and cognitive decline. Hormonal dysfunction is frequent. MRI shows cerebellar white matter abnormalities, as well as brainstem and basal ganglia abnormalities. This so-called "neurodegenerative syndromeg" may occur years before or during manifest histiocytosis and also years after cure. We discovered similar MRI abnormalities in 13 patients and wondered whether they could have the same syndrome. Methods: We reviewed the clinical and laboratory information of these 13 patients and evaluated their brain MRIs. Seven patients underwent spinal cord MRI. Results: All patients were isolated cases; 10 were male. They had signs of cerebellar and pyramidal dysfunction, behavioral problems, and cognitive decline. MRI showed abnormalities of the cerebellar white matter, brainstem, basal ganglia, and, to a lesser extent, cerebral white matter. Three patients had spinal cord lesions. Three patients had laboratory evidence of hormonal dysfunction. No evidence was found of an underlying metabolic defect. In two patients biopsy of nodular brain lesions revealed histiocytic infiltrates. Conclusions: Considering the striking clinical and MRI similarities between our patients and the patients with this neurodegenerative syndrome in the context of proven histiocytosis, it is likely that they share the same paraneoplastic syndrome, although we cannot exclude a genetic disorder with certainty. The fact that we found histiocytic lesions in two patients substantiates our conclusion. Patients with cerebellar white matter abnormalities should be monitored for histiocytosis. © 2008 by AAN Enterprises, Inc