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This paper reports on the compressive properties of a new steel wire– and carbon/glass hybrid fiber–reinforced polymer (S-CG HFRP) bar. The influence of the carbon and glass fiber volume proportion (Vc/Vg), steel wire replacement ratio (Vs), fiber volume ratio (Vf), fiber arrangement, and ratio of the unbraced length to the bar diameter (Lu/d) on the compressive behavior of the S-CG HFRP bars was experimentally investigated. The failure mechanisms were analyzed, revealing that the failure mode changed from fiber microbuckling to fiber macrobuckling with an increase in Lu/d. Adding steel wires resulted in a decrease in the compressive modulus of the S-CG HFRP bars. The compressive strength of the S-CG HFRP bars was not effectively improved by adding steel wires or carbon fibers and was governed by the Lu/d ratio. The results showed that the compressive modulus and strength of the S-CG HFRP bars were approximately 90% and 28% of their tensile modulus and strength, respectively. Finally, the relationship between the compressive and tensile properties of the S-CG HFRP bars was established. Simplified empirical equations were proposed to estimate the compressive strengths of S-CG HFRP bars with different Lu/d ratios. [ABSTRACT FROM AUTHOR]

Background: OTUB1, an essential deubiquitinating enzyme, is upregulated in various types of cancer. Previous studies have shown that OTUB1 may be an oncogene in glioblastoma multiforme (GBM), but its specific regulatory mechanism remains unclear. This study aimed to investigate the mechanism by which OTUB1 and the JAK2/STAT1 signaling pathway co-regulate the growth of GBM. Methods: Using bioinformatics, GBM tissues, and cells, we evaluated the expression and clinical significance of OTUB1 in GBM. Subsequently, we explored the regulatory mechanisms of OTUB1 on malignant behaviors in GBM in vitro and in vivo . In addition, we added the JAK2 inhibitor AZD1480 to explore the regulation of OTUB1 for JAK2/STAT1 pathway in GBM. Results: We found that OTUB1 expression was upregulated in GBM. Silencing OTUB1 promotes apoptosis and cell cycle arrest at G1 phase, inhibiting cell proliferation. Moreover, OTUB1 knockdown effectively inhibited the invasion and migration of GBM cells, and the opposite phenomenon occurred with overexpression. In vivo experiments revealed that OTUB1 knockdown inhibited tumor growth, further emphasizing its crucial role in GBM progression. Mechanistically, we found that OTUB1 was negatively correlated with the JAK2/STAT1 pathway in GBM. The addition of the JAK2 inhibitor AZD1480 significantly reversed the effects of silencing OTUB1 on GBM. Conclusion: Our study reveals a novel mechanism by which OTUB1 inhibits the JAK2/STAT1 signaling pathway. This contributes to a better understanding of OTUB1's role in GBM and provides a potential avenue for targeted therapeutic intervention., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Actin-related protein 2/3 complex subunit 1A (ARPC1A) is implicated in several cancers due to its critical role in regulating actin polymerization. However, the exact mechanism of ARPC1A in cancer remains unclear. This study aims to investigate the biological role of ARPC1A in various cancers and the regulatory role of ARPC1A in glioblastoma multiforme (GBM). We analyzed the expression differences, prognostic value, mutations, immune infiltration, immune microenvironment, and single-cell level correlations of ARPC1A in various cancers. Furthermore, we employed gene set enrichment analysis (GSEA) and functional experiments to elucidate the regulatory mechanisms of ARPC1A on GBM. Importantly, we assessed the role of ARPC1A in temozolomide (TMZ) resistance of GBM. ARPC1A expression was up-regulated in most cancer tissues and was associated with poorer prognosis. Genomic mutation analysis revealed that the predominant type of ARPC1A mutation in tumors was amplification. ARPC1A expression was negatively correlated with B-cell and immune scores in most tumors. Both GSEA and single-cell sequencing have revealed that ARPC1A promotes tumor proliferation and epithelial-mesenchymal transition. In vitro experiments confirmed that ARPC1A knockdown inhibited the proliferation and metastatic ability of GBM cells. Notably, silencing ARPC1A reduced TMZ resistance in GBM cells. This study highlights the prognostic value of ARPC1A in various tumors and its potential for application in immunotherapy. Meanwhile, the modulation of GBM malignant behavior and TMZ resistance by ARPC1A provides a new approach for personalized and precise treatment of GBM., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)