Viologen derivatives have been developeda sn egative electrolyte for neutrala queous organic redox flow batteries (AOFBs), but the structure-performancer elationship remains unclear. Here, it was investigated how the structure of viologens impacts their electrochemical behavior and thereby the battery performance, by taking hydroxylated viologensa se xamples. Calculations of frontierm olecular orbitale nergy and molecular configuration promise to be an effective tool in predicting potential, kinetics, and stability,a nd may be broadly applicable. Specifically,amodified viologen derivative, BHOP-Vi, was provedt ob et he most favorable structure, enablingaconcentrated 2 m battery to exhibit ap owerd ensity of 110.87 mW cm À2 and an excellent capacityr etention rate of 99.953 %h À1 .Renewable energy plays an indispensable role in replacing fossil fuel energy and provides ap ossible solution for as ustainable future. [1] However,t he large-scale adoption of renewable energy,s uch as solar and wind energy,i si mpeded by their intermittent and fluctuating features. The fluctuation in renewable energy supply can be solved by electrochemical energystoraget echnology,w hich stores electricity in electrochemically active materials and provides stable electricity output when needed. [2] As an emerging energy-storage technology,a queous organic redoxf low batteries (AOFBs) exploit the reversible redox reaction of low-cost organic compounds dissolved in aqueous solutions. [3] AOFBs that operate under neutral conditions do not involveh ighly basic or acidic solutionsa nd are therefore safe to handle and have fewer requirementso nb attery components. [4] The electrolyte solutionso faneutralA OFB flow along opposite sides of an ion-selective membrane and are circulated between cell stacksa nd externalt anks. The tanks can be as large as possible to provide long-duration energy supply,a nd the powerc apability can be independently tuned. Powerc apability and cycle lifetime of an eutral AOFB can be effectively tailoredb ye ngineering the chemical structure of redox-active organic electrolytes.Viologens, the characteristicn egative electrolytes (negolytes) for neutral AOFBs, have attracted increasingr esearch interests because of their diverse structure and straightforward chemical modification. The simplest viologen,m ethyl viologen,i sc ommerciallya vailablea nd can also be readily synthesized on a large scale with high yield by reacting bipyridine with either methyli odide or chloroacetic acid. [5] When paired with 4-OH-TEMPO [TEMPO = (2,2,6,6-tetramethylpiperidin-1-yl)oxyl],i tc an deliver ab attery capacity of 13.4 Ah L À1 and ac apacity loss rate of 3.6 %p er day.T his high capacity loss rate is owing to the dimerization of the intermediate, the cationic viologen radical. [6] To prevent the dimerization, Aziz and co-workers took advantage of coulombic repulsion, [7] and after adding quaternary ammonium groups to the viologen core they reporteda much lower capacity loss rate of 0.03 %p er day for the BTMAP-Vi/BTMAP-Fc cell ...

The commonly used general anesthetic isoflurane induces widespread neurodegeneration in the developing mammalian brain through poorly understood mechanisms. We have investigated whether excessive Ca 2ϩ release from the endoplasmic reticulum via overactivation of inositol 1,4,5-trisphosphate receptors (InsP 3 Rs) is a contributing factor in such neurodegeneration in rodent primary cultured neurons and developing rat brain. We also investigated the correlation between isoflurane exposure and cognitive decline in rats at 1 month of age. Our results show that isoflurane increases cytosolic calcium in the primary cortical neurons through release from the endoplasmic reticulum and influx from the extracellular space. Pharmacological inhibition of InsP 3 R activity and knockdown of its expression nearly abolishes the isoflurane-mediated elevation of the cytosolic calcium concentration and cell death in rodent primary cortical and hippocampal neurons. Inhibition of InsP 3 R activity by its antagonist xestospongin C significantly inhibits neurodegeneration induced by isoflurane at clinically used concentration in the developing brain of postnatal day 7 rats. Moreover, our results show that isoflurane activates ␤-site amyloid ␤ precursor protein-cleaving enzyme via activation of the InsP 3 R. We also noted that mice exposed to isoflurane during early postnatal development showed transient memory and learning impairments, which did not correlate well with the noted neuropathological defects. Taken together, our results suggest that Ca 2ϩ dysregulation through overactivation of the InsP 3 R may be a contributing factor in the mechanism of isoflurane-induced neurodegeneration in rodent neuronal cell culture and during brain development.

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