Kyung‐Ho Kim

Abstract Conventional nickel‐rich cathode materials suffer from reaction heterogeneity during electrochemical cycling particularly at high temperature, because of their polycrystalline properties and secondary particle morphology. Despite intensive research on the morphological evolution of polycrystalline nickel‐rich materials, its practical investigation at the electrode and cell levels is still rarely discussed. Herein, an intrinsic limitation of polycrystalline nickel‐rich cathode materials in high‐energy full‐cells is discovered under industrial electrode‐fabrication conditions. Owing to their highly unstable chemo‐mechanical properties, even after the first cycle, nickel‐rich materials are degraded in the longitudinal direction of the high‐energy electrode. This inhomogeneous degradation behavior of nickel‐rich materials at the electrode level originates from the overutilization of active materials on the surface side, causing a severe non‐uniform potential distribution during long‐term cycling. In addition, this phenomenon continuously lowers the reversibility of lithium ions. Consequently, considering the degradation of polycrystalline nickel‐rich materials, this study suggests the adoption of a robust single‐crystalline LiNi 0.8 Co 0.1 Mn 0.1 O 2 as a feasible alternative, to effectively suppress the localized overutilization of active materials. Such an adoption can stabilize the electrochemical performance of high‐energy lithium‐ion cells, in which superior capacity retention above ≈80% after 1000 cycles at 45 °C is demonstrated.

BACKGROUND: Neurodevelopmental disorders are associated with altered patterns of neuronal connectivity. A critical determinant of neuronal connectivity is the dendritic morphology of individual neurons, which is shaped by experience. The identification of environmental exposures that interfere with dendritic growth and plasticity may, therefore, provide insight into environmental risk factors for neurodevelopmental disorders. OBJECTIVE: We tested the hypothesis that polychlorinated biphenyls (PCBs) alter dendritic growth and/or plasticity by promoting the activity of ryanodine receptors (RyRs). METHODS AND RESULTS: The Morris water maze was used to induce experience-dependent neural plasticity in weanling rats exposed to either vehicle or Aroclor 1254 (A1254) in the maternal diet throughout gestation and lactation. Developmental A1254 exposure promoted dendritic growth in cerebellar Purkinje cells and neocortical pyramidal neurons among untrained animals but attenuated or reversed experience-dependent dendritic growth among maze-trained littermates. These structural changes coincided with subtle deficits in spatial learning and memory, increased [3H]-ryanodine binding sites and RyR expression in the cerebellum of untrained animals, and inhibition of training-induced RyR upregulation. A congener with potent RyR activity, PCB95, but not a congener with negligible RyR activity, PCB66, promoted dendritic growth in primary cortical neuron cultures and this effect was blocked by pharmacologic antagonism of RyR activity. CONCLUSIONS: Developmental exposure to PCBs interferes with normal patterns of dendritic growth and plasticity, and these effects may be linked to changes in RyR expression and function. These findings identify PCBs as candidate environmental risk factors for neurodevelopmental disorders, especially in children with heritable deficits in calcium signaling.

OBJECTIVE: Miniscrew-assisted rapid palatal expansion (MARPE) is a means for expanding the basal bone without surgical intervention in young adults. Here, we assessed the differences in dental, alveolar, and skeletal measurements taken before (T0), immediately after (T1), and 1 year after (T2) MARPE. METHODS: -tests: intercusp, interapex, alveolar, nasal floor, and nasal cavity widths; inclination of the first molar (M1) and its alveolus; and thickness and height of the alveolar bone. A linear mixed-effects model was used to determine variables that affected periodontal changes in the M1. RESULTS: MARPE produced significant increases in most measurements during T0-T2, despite relapse of some measurements during T1-T2. The alveolar thickness decreased on the buccal side, but increased on the palatal side. The alveolar crest level at the first premolar moved apically. Changes in the thickness and height of the alveolar bone were affected by the corresponding initial values. CONCLUSIONS: MARPE can be used as an effective tool for correcting maxillomandibular transverse discrepancy, showing stable outcomes 1 year after expansion.