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This article studies the resilient control problem for a class of unknown nonlinear systems with fading measurements under malicious denial-of-service (DoS) attacks. The system output is assumed to be transmitted through a fading channel, where the fading phenomenon is described by a Rice fading model. The strategy of the attacker is to periodically interfere with the networked channels to reduce the success rate of data transmissions. First, a dynamic linearization method along the iteration domain is introduced to convert the nonlinear system into an equivalent data-related model. Then, a model-free adaptive iterative learning control (MFAILC) scheme is presented, which is independent of model information. The convergence of the MFAILC scheme is deduced theoretically and the influence of DoS attacks and stochastic fading phenomenon on system stability are also analyzed. Finally, the effectiveness of the design is verified by a numerical simulation and a trajectory tracking example of wheeled mobile robots (WMRs).

Ni-rich layered oxides are one of the most attractive cathode materials in high-energy-density lithium-ion batteries, their degradation mechanisms are still not completely elucidated. Herein, we report a strong dependence of degradation pathways on the long-range cationic disordering of Co-free Ni-rich Li1-m(Ni0.94Al0.06)1+mO2 (NA). Interestingly, a disordered layered phase with lattice mismatch can be easily formed in the near-surface region of NA particles with very low cation disorder (NA-LCD, m ≤ 0.06) over electrochemical cycling, while the layered structure is basically maintained in the core of particles forming a "core-shell" structure. Such surface reconstruction triggers a rapid capacity decay during the first 100 cycles between 2.7 and 4.3 V at 1 C or 3 C. On the contrary, the local lattice distortions are gradually accumulated throughout the whole NA particles with higher degrees of cation disorder (NA-HCD, 0.06 ≤ m ≤ 0.15) that lead to a slow capacity decay upon cycling.

Deformation mechanisms and magnetic properties of medium and high entropy alloys (MEA/HEAs) closely relate to lattice distortion and are strongly temperature-dependent, in particular, at low temperature ranges. However, little attention has been paid to the evolution of lattice distortion with temperature decreasing and its effects on deformation behavior and magnetic state transition. In this work, we carry out in situ synchrotron radiation based X-ray powder diffraction (SR-XRD) experiments from 293 to 123 K aiming for determining lattice distortion evolutions of CrCoNi MEA, CrFeCoNi and CrMnFeCoNi HEAs. Magnetic measurements at corresponding low temperatures and cryogenic ranges are further conducted. The in situ SR-XRD results demonstrate a general reduction of lattice distortion magnitude with temperature decreasing, which shows a similar tendency with that of reported stacking fault energy (SFE) values. It is thus suggested that lattice distortion reduction possibly makes a critical contribution to deformation mechanism transition. The magnetic measurement results show a clear ferromagnetic transition of CrFeCoNi HEA when temperature is below 173 K. While, no obvious magnetic state transition is observed for CrCoNi MEA and CrMnFeCoNi HEA. The present findings on lattice distortion evolutions will pave the way for designing targeted HEAs with particular properties.

Dynamic miRNA alteration is known to occur in colitis-associated colon cancer (CAC), while the molecular mechanisms underpinning how miRNAs modulate the development from chronic inflammation to CAC is lacking. For the first time, we constructed knockout (KO) mice for individual miR-148/152 family members and entire miR-148/152 family. Based on these KO mice, we conduct the first comprehensive analysis of miR-148/152 family, demonstrating that deficiency of any member of miR-148/152 family aggravate colitis and CAC. Loss of individual miR-148/152 family members or full-family enhance MMP10 and MMP13 expression, causing disruption of intestinal barrier and cleaving pro-TNF-α into bioactive TNF-α fragments to activate NF-κB signaling, thereby aggravating colitis. Individual and full-family deletion also increase accumulation of IKKα and IKKβ, resulting in further hyperactivation of NF-κB signaling, exacerbating colitis and CAC. Moreover, blocking NF-κB signaling exerts a restorative effect on colitis and CAC models only in KO mice. Taken together, these findings demonstrate deleting the full miR-148/152 family or individual members exhibit similar effects in colitis and CAC. Mechanically, miR-148/152 family members deficiency in mice elevates MMP10 and MMP13 to accelerate colitis and CAC via disrupting intestinal barrier function and activating NF-κB signaling, suggesting a potential therapeutic strategy for colitis and CAC.

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