Science Concentrates ENERGY STORAGE
Zinc sponge protects rechargeable battery Unconventional form of zinc electrode leads to low-cost, long-lasting, safe battery To exploit zinc’s useful properties in next-generation batteries, researchers have prepared zinc electrodes in a porous spongelike structure. Batteries with such electrodes could be long-lasting, energy dense, and inherently safe, according to a study (Science 2017, DOI: 10.1126/science.aak9991). The relatively low cost of zinc coupled with its wide availability and favorable electrochemical properties should give zincbased batteries a competitive advantage over other battery chemistries. In particular, Zn batteries could be safer than lithium-ion batteries because Zn ones use aqueous electrolytes instead of the flammable organic kinds standard in Li-ion batteries. But aqueous Zn-based batteries fail quickly. Upon recharging, the metal forms wiry dendrites that can grow uncontrollably and pierce the separator between the electrodes. The dendrites can then connect the positive and negative electrodes and short-circuit the battery. Scientists at the Naval Research Laboratory (NRL) in Washington, D.C., have shown that those problems can be bypassed by using zinc electrodes with a spongelike structure instead of conventional pressed powder electrodes.
The team, which includes Joseph F. Parker, Debra R. Rolison, and Jeffrey W. Long, prepared the zinc sponges by adding zinc powder to an emulsion of oil and water and then allowing the mixture to dry overnight. The sponge structure leads to more uniform oxidation of the zinc metal during discharge and, consequently, a more uniform coating of the discharge product, zinc oxide, on the sponge anode. Likewise, the structure makes the reverse reaction during charging—ZnO reduction to metallic Zn—more uniform. Even when 90% of the zinc is oxidized during discharge, Parker notes, the sponge retains a metallic zinc core. The core causes electric currents to be distributed uniformly throughout the sponge, making it physically difficult to form dendrites, he adds. The team found that the sponge electrodes protected a Ni-Zn battery when it cycled repeatedly between charging and discharging under demanding current conditions that induce dendrite formation in reference batteries. It also enabled the battery to withstand tens of thousands of cycles required for “start-stop” microhybrid vehicles.
Unlike conventional zinc powder anodes (left), spongelike zinc anodes resist dendrite formation (right). “For quite some time, this team and others have been attempting to use 3-D structured electrodes to enhance rechargeable battery performance,” says Paul V. Braun, professor of materials science and chemistry at the University of Illinois, Urbana-Champaign. Braun notes that the NRL team “has found a particularly compelling system, where the 3-D electrode structure provides high power, as expected, but perhaps surprisingly, results in dendrite suppression and thus very good long term cycling.” He adds “this discovery is particularly useful because it is accomplished with an intrinsically safe, earth abundant, and relatively high-energy-density nickel-zinc chemistry.”—MITCH JACOBY
NEUROSCIENCE
CREDIT: SCIENCE
Finding a role for polyglutamine In nine neurodegenerative diseases, the culprit is an increase in the number of repeated glutamines in a certain protein. For example, healthy people have between six and 35 glutamines in a row in their huntingtin proteins, whereas people with Huntington’s disease can have more than 100. With these expanded polyglutamine (polyQ) tracts, the proteins tend to aggregate, but scientists don’t know how the mutant proteins cause neurodegeneration when they’re instead floating freely around cells. Now a team of researchers reports that the nonexpanded polyQ tract of one protein
helps regulate how cells dispose of their molecular garbage. The findings also suggest that expanded tracts associated with disease might disrupt that disposal process (Nature 2017, DOI: 10.1038/nature22078). Cells trigger a process called autophagy to clear out aggregated proteins, lipids, and other—possibly toxic—junk in their cytoplasm. David C. Rubinsztein of the University of Cambridge and colleagues found that when they decreased expression of a protein called ataxin-3 in cells, autophagy slowed. Ataxin-3 has a polyQ tract, and expansion of it leads to the neurodegenerative disease spinocerebellar ataxia type 3. Ru-
binsztein’s team found that normal ataxin-3 keeps autophagy running smoothly by protecting a key autophagy protein called beclin-1 from degradation. To do this, ataxin-3’s polyQ tract first binds to beclin-1. The scientists determined that longer polyQ tracts—such as those in disease versions of huntingtin—bind beclin-1 more strongly, outcompeting normal ataxin-3. As a result, beclin-1 levels drop and autophagy slows in the cells. When studying cells derived from patients with Huntington’s disease, the scientists found that rates of autophagy also were decreased.—MICHAEL
TORRICE MAY 1, 2017 | CEN.ACS.ORG | C&EN
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