High-Ni layered oxide cathode is considered as one of the most promising cathodes for high-energydensity lithium-ion batteries due to its high capacity and low cost. However, surficial residues, such as NiO-type rock-salt phase and Li 2 CO 3 , are often formed at the particle surface due to the high reactivity of Ni 3+ , and inevitably result in an inferior electrochemical performance, hindering the practical application. Herein, unprecedentedly clean surfaces without any surficial residues are obtained in a representative LiNi 0.8 Co 0.2 O 2 cathode by Ti gradient doping. High-resolution TEM reveals that the particle surface is composed of disordered layered phase (~ 6 nm in thickness) with the same rhombohedra structure as its interior. The formation of this disordered layered phase at the particle surface is electrochemically-favored. It leads to the highest rate capacity ever reported and a superior cycling stability. First-principles calculations further confirm that the excellent electrochemical performance roots in the great chemical/structural stability of such a disordered layered structure, mainly arising from the improved robustness of the oxygen framework by Ti doping. This strategy of constructing the disordered layered phase at the particle surface could be extended to other high-Ni layered transition metal oxides, which will contribute to the enhancement of their electrochemical performance. Received: ((will be filled in by the editorial staff)) Revised: ((will be filled in by the editorial staff))

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Background/Aims: The biological effects of periodic mechanical stress on chondrocytes have been studied extensively over the past few years. However, the mechanisms underlying chondrocyte mechanosensing and signaling in response to periodic mechanical stress remain to be determined. In the current study, we examined the effects of focal adhesion kinase (FAK) signaling on periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis. Methods and Results: Periodic mechanical stress significantly induced sustained phosphorylation of FAK at Tyr³⁹⁷ and Tyr^576/577. Reduction of FAK with targeted shRNA via transfection of NH₂-terminal tyrosine phosphorylation-deficient FAK mutant Y397F or Y576F-Y577F abolished periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis, accompanied by attenuated ERK1/2 phosphorylation. However, activation of Src, PLCγ1 and Rac1 was not prevented upon FAK suppression. Furthermore, pretreatment with the Src-selective inhibitor, PP2, and shRNA targeted to Src or suppression of Rac1 with its selective inhibitor, NSC23766, blocked FAK phosphorylation at Tyr,^576/577 but not Tyr,³⁹⁷ under periodic mechanical stress. Interestingly, FAK phosphorylation neither at Tyr³⁹⁷ nor at Tyr^576/577 was affected by PLCγ1 depletion when periodic mechanical stress was applied. In addition, Tyr³⁹⁷ and Tyr^576/577 phosphorylation levels were reduced upon pretreatment with a blocking antibody against integrin β1 under conditions of periodic mechanical stress. Conclusion: Our findings collectively suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis through at least two pathways, integrin β1-Src-Rac1-FAK(Tyr^576/577)-ERK1/2 and integrin β1-FAK (Tyr³⁹⁷)-ERK1/2.