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Although there are lots of researches about the application of FRP composites on the external bonding and reinforcement of timber structures, they are mostly aimed at Carbon FRP, which has a large difference in mechanical properties and inconsistent deformation with timber. Meanwhile, research about the interface between timber and Flax Fiber Reinforced Polymer (FFRP) with similar properties with timber is limited; hence, relevant models have not been established yet. Similar to linear elastic FRP confined timber structure, the failure of FFRP-timber structure interface is a process in which the interfacial stress is gradually transferred from the loaded end to the free end, and the interfacial stress transfer area, that is an effective bond length of the FFRP-timber interface. In order to study the interfacial stress transfer characteristics between FFRP and timber structure, based on the existing CFRP-timber structure interface bonding theory and mechanism, a single lap shear test is used to conduct a systematic study on bonding length and width are studied to optimized the application of FFRP. The bond-slip behavior is studied and fitted to provide theory support for the application of FFRP in the restoration of ancient timber structures.

Abstract Secondary trastuzumab resistance represents an evolutionary adaptation of HER2‐positive breast cancer during anti‐HER2 treatment. Most current studies have tended to prioritize HER2 and its associated signaling pathways, often overlooking broader but seemingly less relevant cellular processes, along with their associated genetic and epigenetic mechanisms. Here, transcriptome data is not only characterized but also examined epigenomic and 3D genome architecture information in both trastuzumab‐sensitive and secondary‐resistant breast cancer cells. The findings reveal that the global metabolic reprogramming associated with trastuzumab resistance may stem from genome‐wide alterations in both histone modifications and chromatin structure. Specifically, the transcriptional activities of key genes involved in lipid metabolism appear to be regulated by variant promoter H3K27me3 and H3K4me3 modifications, as well as promoter‐enhancer interactions. These discoveries offer valuable insights into how cancer cells adapt to anti‐tumor drugs and have the potential to impact future diagnostic and treatment strategies.

Abstract As a key regulator of the DNA translesion synthesis (TLS) pathway, RAD18 is error-prone and contributes to the accumulation of DNA mutations. Our previous study showed that it plays an essential role in the progression of multiple tumors. However, the mechanism through which RAD18 influences triple-negative breast cancer (TNBC), especially the interaction between tumor cells and the tumor microenvironment, remains elusive. In this study, we showed that RAD18 expression is markedly higher in patients with high T stage TNBC and inversely correlated with prognosis. High expression of RAD18 facilitated a highly stem-cell phenotype through the Hippo/YAP pathway, which supports the proliferation of TNBC. In addition, the cytokine byproduct TGF-β activates macrophages to have an M2-like tumor-associated macrophage (TAM) phenotype. Reciprocally, TGF-β from TAMs activated RAD18 in TNBC to enhance tumor stemness, forming a positive feedback loop. Inhibition of YAP or TGF-β breaks this loop and suppresses cancer stemness and proliferation In nude mice, RAD18 promoted subcutaneous transplanted tumor growth and M2-type TAM recruitment. Collectively, the RAD18-YAP-TGF-β loop is essential for the promotion of the stemness phenotype by TNBC and could be a potential therapeutic target for TNBC.