MoS2@ZnO Nanoheterostructures Prepared by Electrospark Erosion for Photocatalytic Applications

MoS2@ZnO nanoheterostructures were synthesized by electrospark erosion of zinc granules in a hydrogen peroxide solution and simultaneous addition of MoS2 nanostructured powder into the reaction zone. The morphology, size of the crystallites, as well as elemental and phase composition of the prepared structures, were examined using transmission electron microscopy and X-ray diffraction analysis. It was found that the synthesized products represent heterostructures containing MoS2 nanoparticles formed on ZnO nanoparticles. Raman spectroscopy and photoluminescence analysis were also used for characterization of the prepared heterostructures. The obtained MoS2@ZnO nanostructures revealed an intense broad emission band ranging from 425 to 625 nm for samples with different fractions of MoS2. Photocatalytic measurements showed that the maximal hydrogen evolution rate of the prepared nanoheterostructures was about 906.6 μmol·g−1·h−1. The potential of their application in photocatalytic water splitting was also estimated

ELECTROENCEPHALOGRAPHIC CHANGES WITH DRAVET SYNDROME

Dravet syndrome (DS, severe myoclonic epilepsy of early infancy) is epileptic encephalopathy with onset in the first year of life, manifested with febrile and afebrile generalized and focal seizures, with the presence of myoclonic paroxysms in typical cases, mental retardation, and resistance to antiepileptic therapy. The disease was for the first time described by Ch. Dravet in 1978 in France, then, in details, by Сh. Dravet et al. in 1982. In the classification of 1989, DS held a particular place being attributed to the forms of epilepsy that have both generalized and focal clinical manifestations. According to Proposed diagnostic scheme for people with epileptic seizures and with epilepsy (2001), this disease is attributed to epileptic encephalopathies of early infancy. The main reason of DS development is a mutation in the SCN1A gene revealed with most (but not all) patients. It is assumed that there are certain other mutations that determine DS development, in particular, the GABRG2 mutation. Polymorphism of epileptic seizures is typical of the DS: febrile seizures, focal motor (including hemiclonic and secondarily generalized), generalized tonic and clonic, alternating hemiconvulsions, myoclonic, atypical absences, focal dialeptic seizures, as well as epileptic status. The prognosis of the disease is severe. In most cases, seizures continue to occur in adult life but with lower frequency than in childhood. The authors review the issues of etiology and pathogenesis in details, as well as clinical manifestations, diagnostics, and treatment of the DS. A particular emphasis is given to pathological changes on electroencephalogram (EEG) of patients with DS. Distinct slowing of background activity, prevalence of multiregional epileptiform activity, regional slowing, and severe photosensitivity (pattern sensitivity) are the most prognostically unfavorable EEG patterns of the DS