In this work, we have developed a non-ordinary state-based peridynamic model for multiple crack initiation and propagation due to compression-compression fatigue load. In each loading cycle, the fatigue loading is redistributed among the peridynamic solid body, leading to the progressive fatigue damage initiation and propagation in an autonomous fashion. The proposed fatigue model parameters are firstly validated by 3D numerical benchmark tests, and then it is applied to simulate widespread fatigue damage evolution of the aircraft wing corner box. The modified constitutive damage model has been implemented into the peridynamics framework at finite strain. Furthermore, the criterion algorithm from multiple initiation to propagation is discussed. It is shown that the numerical results obtained from peridynamics simulations are in general agreement with those from the experiment data. The comparison of experimental and numerical results indicates that the proposed non-ordinary state-based peridynamics fatigue model has the ability to capture the multiple crack initiation and propagation and other features of the aluminium alloy material.

Low-grade glioma (LGG) is a highly aggressive disease in the skull. On the other hand, anoikis, a specific form of cell death induced by the loss of cell contact with the extracellular matrix, plays a key role in cancer metastasis. In this study，anoikis-related genes (ANRGs) were used to identify LGG subtypes and to construct a prognostic model for LGG patients. In addition, we explored the immune microenvironment and enrichment pathways between different subtypes. We constructed an anoikis-related gene signature using the TCGA cohort and investigated the differences in clinical features, mutational landscape, immune cell infiltration, etc. between different risk groups. Kaplan-Meier analysis showed that the characteristics of ANRGs in the high-risk group were associated with poor prognosis in LGG patients. The risk score was identified as an independent prognostic factor. The high-risk group had higher immune cell infiltration, tumor mutation load, immune checkpoint gene expression, and ICB treatment response. Functional analysis showed that these high- and low-risk groups had different immune statuses and drug sensitivity. Risk scores were used together with LGG clinicopathological features to construct a nomogram, and DCA analysis showed that the model could enable patients to benefit from clinical treatment strategies.