ALBERT

Description: In order to develop long-lifespan batteries, it is of utmost importance to identify the relevant aging mechanisms and their relation to operating conditions. The capacity loss in a lithium-ion battery originates from (i) a loss of active electrode material and (ii) a loss of active lithium. The focus of this work is the capacity loss caused by lithium loss, which is irreversibly bound to the solid electrolyte interface (SEI) on the graphite surface. During operation, the particle surface suffers from dilation, which causes the SEI to break and then be rebuilt, continuously. The surface dilation is expected to correspond with the well-known graphite staging mechanism. Therefore, a high-power 2.6 Ah graphite/LiNiCoAlO2 cell (Sony US18650VTC5) is cycled at different, well-defined state-of-charge (SOC) ranges, covering the different graphite stages. An open circuit voltage model is applied to quantify the loss mechanisms (i) and (ii). The results show that the lithium loss is the dominant cause of capacity fade under the applied conditions. They experimentally prove the important influence of the graphite stages on the lifetime of a battery. Cycling the cell at SOCs slightly above graphite Stage II results in a high active lithium loss and hence in a high capacity fade.

Description: Many reports detail taste dysfunction in humans and animals with obesity. For example, mice consuming an obesogenic diet for a short period have fewer taste buds than their lean littermates. Further, rats with diet-induced obesity (DIO) show blunted electrophysiological responses to taste in the brainstem. Here, we studied the effects of high energy diet (HED)-induced peripheral taste damage in rats, and whether this deficiency could be reversed by returning to a regular chow diet. Separate groups of rats consumed a standard chow diet (Chow), a HED for 10 weeks followed by a return to chow (HED/chow), or a HED for 10 weeks followed by a restricted HED that was isocaloric with consumption by the HED/chow group (HED/isocal). Fungiform taste papilla (FP) and circumvallate taste bud abundance were quantified several months after HED groups switched diets. Results showed that both HED/chow and HED/isocal rats had significantly fewer FP and lower CV taste bud abundance than control rats fed only chow. Neutrophil infiltration into taste tissues was also quantified, but did not vary with treatment on this timeline. Finally, the number of cells undergoing programmed cell death, measured with caspase-3 staining, inversely correlated with taste bud counts, suggesting taste buds may be lost to apoptosis as a potential mechanism for the taste dysfunction observed in obesity. Collectively, these data show that DIO has lasting deleterious effects on the peripheral taste system, despite a change from a HED to a healthy diet, underscoring the idea that obesity rather than diet predicts damage to the taste system.