Is Ba3In2O6a high-Tcsuperconductor?

It has been suggested that Ba3In2O6might be a high-Tcsuperconductor. Experimental investigation of the properties of Ba3In2O6was long inhibited by its instability in air. Recently epitaxial Ba3In2O6with a protective capping layer was demonstrated, which finally allows its electronic characterization. The optical bandgap of Ba3In2O6is determined to be 2.99 eV in-the (001) plane and 2.83 eV along thec-axis direction by spectroscopic ellipsometry. First-principles calculations were carried out, yielding a result in good agreement with the experimental value. Various dopants were explored to induce (super-)conductivity in this otherwise insulating material. NeitherA- norB-site doping proved successful. The underlying reason is predominately the formation of oxygen interstitials as revealed by scanning transmission electron microscopy and first-principles calculations. Additional efforts to induce superconductivity were investigated, including surface alkali doping, optical pumping, and hydrogen reduction. To probe liquid-ion gating, Ba3In2O6was successfully grown epitaxially on an epitaxial SrRuO3bottom electrode. So far none of these efforts induced superconductivity in Ba3In2O6,leaving the answer to the initial question of whether Ba3In2O6is a high-Tcsuperconductor to be 'no' thus far.

Mutations in the IRBIT domain of ITPR1 are a frequent cause of autosomal dominant nonprogressive congenital ataxia.

Congenital ataxias are nonprogressive neurological disorders characterized by neonatal hypotonia, developmental delay and ataxia, variably associated with intellectual disability and other neurological or extraneurological features. We performed trio-based whole-exome sequencing of 12 families with congenital cerebellar and/or vermis atrophy in parallel with targeted next-generation sequencing of known ataxia genes (CACNA1A, ITPR1, KCNC3, ATP2B3 and GRM1) in 12 additional patients with a similar phenotype. Novel pathological mutations of ITPR1 (inositol 1,4,5-trisphosphate receptor, type 1) were found in seven patients from four families (4/24, ∼16.8%) all localized in the IRBIT (inositol triphosphate receptor binding protein) domain which plays an essential role in the regulation of neuronal plasticity and development. Our study expands the mutational spectrum of ITPR1-related congenital ataxia and indicates that ITPR1 gene screening should be implemented in this subgroup of ataxias.

Early development of epileptic infants with pre- or perinatal brain injuries: role of the epileptic disorder.

To try to understand the causative role of epilepsy PER SE in the developmental deterioration of brain injured infants, twenty-eight infants affected with early acquired, pre- and perinatal brain injuries were enrolled and divided into three groups, a) those with West syndrome, b) those with other non-West epilepsies, and c) those without epilepsy. Developmental monitoring consisted of a full clinical assessment, including examination of visual function, Griffiths developmental scales, standard EEG, long-term monitoring when necessary, and MRI, from the seizure onset or the first observation to the end of follow-up. Patients with epilepsy showed at study onset abnormal clinical features (neurological and developmental) distinct from those of non-epileptic patients, partially due to the varying severity of their brain injuries. A definite differentiation between groups was observed in the clinical evolution that showed among the epileptic patients, mostly in West syndrome, a significant deterioration. Moreover, impaired visual function at seizure onset was possibly associated with a bad developmental evolution. A developmental deterioration, mostly in West syndrome, accounts for a causative role of the epileptic disorder PER SE, but in few cases it was also observed in infants with only a brain injury, suggesting other aetiopathogenic mechanisms. The predictive value of early visual function seems to be confirmed.