Short-term Breakdown and Long-term Failure in Nanodielectrics: A Review

Nanodielectrics, which are concentrated in polymer matrix incorporating nanofillers, have received considerable attention due to their potential benefits as dielectrics. In this paper, short-term breakdown and long-term failure properties of nanodielectrics have been reviewed. The characteristics of polymer matrix, types of nanoparticle and its content, and waveforms of the applied voltage are fully evaluated. In order to effectively comment on the published experimental data, a ratio k has been proposed to compare the electric properties of the nanodielectrics with the matrix and assess the effect for nanoparticles doping. There is evidence that the short-term breakdown properties of nanodielectrics show a strong dependence on the applied voltage waveforms. The polarity and the cohesive energy density (CED) of polymer matrix have a dramatic influence on the properties of nanodielectrics. Nanoparticle doped composites show a positive effect on the long-term failure properties, such as ageing resistance and partial discharge (PD) properties of nanocomposites are superior than microcomposites and the matrix. The larger the dielectric constant and CED of the matrix become, the more significant improvements in long-term performance appear. Based on the reported experimental results, we also present our understandings and propose some suggestions for further work

Aberrant Calcium Signaling in Astrocytes Inhibits Neuronal Excitability in a Human Down Syndrome Stem Cell Model

Down syndrome (DS) is a genetic disorder that causes cognitive impairment. The staggering effects associated with an extra copy of human chromosome 21 (HSA21) complicates mechanistic understanding of DS pathophysiology. We examined the neuron-astrocyte interplay in a fully recapitulated HSA21 trisomy cellular model differentiated from DS-patient-derived induced pluripotent stem cells (iPSCs). By combining calcium imaging with genetic approaches, we discovered the functional defects of DS astroglia and their effects on neuronal excitability. Compared with control isogenic astroglia, DS astroglia exhibited more-frequent spontaneous calcium fluctuations, which reduced the excitability of co-cultured neurons. Furthermore, suppressed neuronal activity could be rescued by abolishing astrocytic spontaneous calcium activity either chemically by blocking adenosine-mediated signaling or genetically by knockdown of inositol triphosphate (IP3) receptors or S100B, a calcium binding protein coded on HSA21. Our results suggest a mechanism by which DS alters the function of astrocytes, which subsequently disturbs neuronal excitability