Enterovirus 71 (EV71) causes epidemics of hand, foot, and mouth disease associated with neurological complications in young children. We report an outbreak of EV71-associated neurological disease that occurred from February through September 1999 in Perth, Western Australia. Fourteen children with culture-proven, EV71-induced neurological disease were identified. Nine patients (64%) developed severe neurological disease; 4 of these patients developed long-term neurological sequelae. Neurological syndromes included aseptic meningitis, Guillain-Barré syndrome, acute transverse myelitis, acute cerebellar ataxia, opso-myoclonus syndrome, benign intracranial hypertension, and a febrile convulsion. Clinical and magnetic resonance imaging data indicated that immunopathology was a major factor in the pathogenesis of neurological disease in this outbreak. This finding is in contrast to reports of previous EV71 epidemics, in which virus-induced damage to gray matter was the most frequent cause of neurological disease.

Insulator-metal transitions are well known in transition metal oxides, but inducing an insulator-metal transition in the oxide of a main group element is a major challenge. Here we report the observation of an insulator-metal transition, with a conductivity jump of seven orders of magnitude, in highly non-stoichiometric, amorphous gallium oxide of approximate composition GaO 1.2 at a temperature around 670 K. We demonstrate through experimental studies and density-functional-theory calculations that the conductivity jump takes place at a critical gallium concentration and is induced by crystallization of stoichiometric Ga 2 O 3 within the metastable oxide matrix -in chemical terms by a disproportionation. This novel mechanism -an insulator-metal transition driven by a heterogeneous solid state reactionopens up a new route to achieve metallic behaviour in oxides that are expected to exist only as classic insulators.Insulator-metal transitions belong to the most fascinating phenomena in condensed-matter physics 1,2 . Since Mott's landmark work 3,4 it has been known that in crystalline solids strong electron-electron interactions can cause an insulator-metal transition. One example is crystalline Cr-doped vanadium oxide, (V 1-x Cr x ) 2 O 3 , which shows a Mott transition from a paramagnetic Mott insulator to a strongly correlated metal upon an increase in pressure, a lowering of temperature, or a decrease in dopant level 5,6 . In non-crystalline solids structural disorder can also lead to an insulator-metal transition on account of Anderson localization 7 .As shown by Anderson 7 and Mott 8 , in any non-crystalline material the lowest states in the conduction band are localized, i.e. they are electron traps. Only for energies above the mobility edge, E c , do states become non-localized or extended. If the Fermi energy E F is below the mobility edge, states at the Fermi level are localized and the material is an electronic insulator. If, however, the number of electrons increases and the Fermi energy rises above the mobility edge, the material becomes metallic (Anderson transition). As transition metals change their valence state easily, most examples of insulator-metal transitions concern transition metal compounds 4-6,9-11 . The above considerations do not, however, exclude the possibility of inducing an insulator-metal transition in a simple binary oxide of a main group element, even without doping. Instead, large deviations from the ideal stoichiometry, i.e. high defect concentrations, provide a high concentration of electronic defects (self-doping). And if, in addition, the oxide is amorphous, there are two phenomena, strong structural disorder and strong chemical disorder, which could result in an insulator-metal transition.Here we report such a case: Highly non-stoichiometric, amorphous gallium oxide with an approximate chemical composition GaO 1.2 shows an unprecedented insulator-metal transition, with a jump in conductivity of ca. 7 orders of magnitude at temperatures as high as 670 K. We show that this in...

Rett syndrome (RTT) is a severe neurological disorder, affecting mainly females. It is generally caused by mutations in the MECP2 gene. Sleep problems are thought to occur commonly in Rett syndrome, but there has been little research on prevalence or natural history. An Australian population-based registry of cases born since 1976 has been operating since 1993, with current ascertainment at 300. The Australian Rett Syndrome Database (ARSD) consists of information about Rett syndrome cases including their functional ability, behaviour, sleep patterns, medical conditions and genotype. The cases range in age from two to 29 years.The aim of this study was to investigate the type and frequency of sleep problems, relationships with age and MECP2 mutation type and to evaluate changes over time.Parents or carers of the subjects with Rett syndrome were asked to complete a questionnaire about sleep problems on three separate occasions (2000, 2002 and 2004). Regression modelling was used to investigate the relationships between sleep problems, age and mutation type. Sleep problems were identified in over 80% of cases. The prevalence of night-time laughter decreased with age and the prevalence of reported night-time seizures and daytime napping increased with age. The prevalence of sleep problems was highest in cases with a large deletion of the MECP2 gene and in those with the p.R294X or p.R306C mutations.Sleep problems are common in Rett syndrome and there is some variation with age and mutation type.