Mitigating the Kinetic Hindrance of Single-Crystalline Ni-Rich Cathode via Surface Gradient Penetration of Tantalum.

Single-crystalline Ni-rich cathodes are promising candidates for the next-generation high-energy Li-ion batteries. However, they still suffer from poor rate capability and low specific capacity due to the severe kinetic hindrance at the nondilute state during Li+ intercalation. Herein, combining experiments with density functional theory (DFT) calculations, we demonstrate that this obstacle can be tackled by regulating the oxidation state of nickel via injecting high-valence foreign Ta5+ . The as-obtained single-crystalline LiNi0.8 Co0.1 Mn0.1 O2 delivers a high specific capacity (211.2 mAh g-1 at 0.1 C), high initial Coulombic efficiency (93.8 %), excellent rate capability (157 mAh g-1 at 4 C), and good durability (90.4 % after 100 cycles under 0.5 C). This work provides a strategy to mitigate the Li+ kinetic hindrance of the appealing single-crystalline Ni-rich cathodes and will inspire peers to conduct an intensive study.

Osteopontin stimulates autophagy via integrin/CD44 and p38 MAPK signaling pathways in vascular smooth muscle cells.

Osteopontin (OPN) exerts pro-inflammatory effect and is associated with the development of abdominal aortic aneurysm (AAA). However, the molecular mechanism underlying this association remains obscure. In the present study, we compared gene expression profiles of AAA tissues using microarray assay, and found that OPN was the highest expressed gene (>125-fold). Furthermore, the expression of LC3 protein and autophagy-related genes including Atg4b, Beclin1/Atg6, Bnip3, and Vps34 was markedly upregulated in AAA tissues. To investigate the ability of OPN to stimulate autophagy as a potential mechanism involved in the pathogenesis of this disease, we treated vascular smooth muscle cells (SMCs) with OPN, and found that OPN significantly increased the formation of autophagosomes, expression of autophagy-related genes and cell death, whereas blocking the signal by anti-OPN antibody markedly inhibited OPN-induced autophagy and SMC death. Furthermore, inhibition of integrin/CD44 and p38 MAPK signaling pathways markedly abrogated the biological effects of OPN on SMCs. These data for the first time demonstrate that OPN sitmulates autophagy directly through integrin/CD44 and p38 MAPK-mediated pathways in SMCs. Thus, inhibition of OPN-induced autophagy might be a potential therapeutic target in the treatment of AAA disease. J. Cell. Physiol. 227: 127-135, 2012. © 2011 Wiley Periodicals, Inc.