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Electrochemical capacitors featuring a modified acetonitrile (AN) electrolyte and a binder-free, activated carbon fabric electrode material were assembled and tested at <−40 °C. The melting point of the electrolyte was depressed relative to the standard pure AN solvent through the use of a methyl formate cosolvent, to enable operation at temperatures lower than the rated limit of typical commercial cells (−40 °C). Based on earlier electrolyte formulation studies, a 1:1 ratio of methyl formate to AN (by volume) was selected, to maximize freezing point depression while maintaining a sufficient salt solubility. The salt spiro-(1,1′)-bipyrrolidinium tetrafluoroborate was used, based on its improved conductivity at low temperatures, relative to linear alkyl ammonium salts. The carbon fabric electrode supported a relatively high rate capability at temperatures as low as −65 °C with a modest increase in cell resistance at this reduced temperature. The capacitance was only weakly dependent on temperature, with a specific capacitance of ∼110 F/g.
Hopes to identify genetic susceptibility loci accounting for the heritability seen in unipolar depression have not been fully realized. Family history remains the ‘gold standard’ for both risk stratification and prognosis in complex phenotypes such as depression. Meanwhile, the physiological mechanisms underlying life-event triggers for depression remain opaque. Epigenetics, comprising heritable changes in gene expression other than alterations of the nucleotide sequence, may offer a way to deepen our understanding of the aetiology and pathophysiology of unipolar depression and optimize treatments. A heuristic target for exploring the relevance of epigenetic changes in unipolar depression is the hypothalamic–pituitary–adrenal (HPA) axis. The glucocorticoid receptor (GR) gene (NR3C1) has been found to be susceptible to epigenetic modification, specifically DNA methylation, in the context of environmental stress such as early life trauma, which is an established risk for depression later in life.
In this paper we discuss the progress that has been made by studies that have investigated the relationship between depression, early trauma, the HPA axis and the NR3C1 gene. Difficulties with the design of these studies are also explored.
Future efforts will need to comprehensively address epigenetic natural histories at the population, tissue, cell and gene levels. The complex interactions between the epigenome, genome and environment, as well as ongoing nosological difficulties, also pose significant challenges.
The work that has been done so far is nevertheless encouraging and suggests potential mechanistic and biomarker roles for differential DNA methylation patterns in NR3C1 as well as novel therapeutic targets.
Sir George Smart (1776–1867), conductor, composer, singing teacher and organist, was a central figure in nineteenth-century British musical life. He is best remembered as one of the founder members of the Philharmonic Society, for which he often conducted. Notably, in 1826 he presided over the first performance in England of Beethoven's ninth symphony. Smart was also much in demand as a conductor at the major English musical festivals and on royal occasions. These edited journal entries, first published in 1907, provide insightful accounts of concert life at the time, and they are particularly valuable for Smart's detailed observations - gathered during his extensive tour of 1825 - on musical practice in Europe, including conducting methods and performing speeds. The journal extracts end in 1845 with an account of Smart's visit to Bonn for the unveiling of Beethoven's statue.