Toward adequate control of internal interfaces utilizing nitrile-based electrolytes.

Methods to control internal interfaces in lithium ion batteries often require sophisticated procedures to deposit coating layers or introduce interphases, which are typically difficult to apply. This particularly holds for protection from parasitic reactions at the current collector, which reflects an internal interface for the electrode composite material and the electrolyte. In this work, electrolyte formulations based on aliphatic cyclic nitriles, cyclopentane-1-carbonitrile and cyclohexane-1-carbonitrile, are introduced that allow for successful suppression of aluminum dissolution and control of internal interfaces under application-relevant conditions. Such nitrile-based electrolytes show higher intrinsic oxidative and thermal stabilities as well as similar capacity retentions in lithium nickel-manganese-cobalt oxide LiNi3/5Mn1/5Co1/5O2 (NMC622)||graphite based full cells compared to the state-of-the-art organic carbonate-based electrolytes, even when bis(trifluoro-methane)sulfonimide lithium salt is utilized. Moreover, the importance of relative permittivity, degree of ion dissociation, and viscosity of the applied electrolyte formulations for the protection of current collector interfaces is emphasized.

Increased risk of experimental central nervous system listeriosis in rats with chronic serum sickness. An immunohistopathological study.

The incidence and severity of central nervous system (CNS) infection were increased following the intraperitoneal innoculation of Listeria monocytogenes in adult Wistar rats with experimental chronic serum sickness. The results were attributed to an alteration in the blood-cerebrospinal fluid barrier induced by immune complex deposits in the choroid plexus of animals hyperimmunized with bovine serum albumin. CNS inflammation occurred in 16 of 40 (40%) of the test animals studied; one of 36 (2.8%) controls had CNS inflammation. There were extensive pathological changes in the choroid plexus, subarachnoid space, and neural parenchyma of the test animals, as compared with only small inflammatory foci limited to the choroid plexus and subarachnoid space in the one affected control. This experimental model for inducing bacterial CNS infection simulates certain predisposing conditions in chronic immune disease, and may therefore be useful in studying the pathogenesis of CNS infection in such cases.