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The mechanism of steel corrosion in recycled brick powder (RBP)–incorporated concrete remains unclear considering the potential utilization of active RBP for low-carbon design in engineering structures. This study aimed to point the influence of RBP on the corrosion behavior of reinforced concrete under the action of chloride or carbonation. Mortar containing RBP (RBPM) was used in this study to concentrate on the effect of RBP and limit the effect of coarse aggregate. The mechanical, chloride penetration, and carbonation properties of RBPM were first investigated. Then the steel corrosion in reinforced RBPM under the action of chloride or carbonation was evaluated by different electrochemical tests. The underlying mechanisms were elucidated by the chemical composition, pH value, and pore structures of RBPM. The results showed that the compressive strength of mortar decreased 21.7% when 30% RBP was used. The addition of RBP reduced the chloride ion permeability but increased the carbonation depth of RBPM. The corrosion caused by chloride penetration in reinforced RBPM was reduced with a higher corrosion potential and lower corrosion current density, which resulted in an approximately 20% lower mass loss with 30% RBP. However, compared with normal concrete, RBPM suffered an increase in corrosion after carbonation. The corrosion current density and mass loss were greatly increased with increasing the RBP content. When the replacement ratio of RBP was 20%, the mortar was in low corrosion state after carbonation curing for 56 days. This was because a combination of the pozzolanic, filling, and nucleation effect of RBP contributed to a 16.28% lower cumulative pore volume and lower pH of RBPM. Considering the effect of RBP on the mechanical properties and corrosion of reinforce mortar, this study suggested a utilization ratio of 20% for RBP in the practical project. [ABSTRACT FROM AUTHOR]

In the dynamic landscape of cervical cancer (CC) pathophysiology, this study aimed to elucidate the role of necroptosis in modulating tumor proliferation, invasion, and the immune microenvironment in CC. In this study, the impact of necroptosis on CC was evaluated through a series of bioinformatical analyses and experimental approaches. The impact of necroptosis on CC was illustrated by analyzing its effects on tumor aggression, immune responses, and the JAK2-STAT3 signaling pathway. Bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), was also evaluated for its potential induction of necroptosis in CC cells and its interaction with necroptosis inhibitors. Additionally, the study assessed the influence of necroptosis on the immune microenvironment, particularly in T-cell-related pathways and the expression of tumor suppressor genes in CC. Necroptosis was found to enhance VEGFA expression through the activation of the JAK2-STAT3 pathway, promoting tumor proliferative and invasive capabilities in CC. Bevacizumab induced necroptosis in CC cells, potentially leading to resistance to therapy. The combination of bevacizumab with necroptosis inhibitors attenuated VEGFA expression, suggesting a novel therapeutic strategy. Additionally, necroptosis activated T-cell-related pathways and promoted the infiltration and activation of Jurkat T cells. CD3D-a tumor suppressor gene in CC-was identified as a critical marker and its expression could be upregulated by necroptosis via the JAK2-STAT3 pathway in Jurkat T cells. Treatment of CC cells with supernatants from necroptosis-induced Jurkat cells resulted in reduced tumor cell proliferation and invasion. This study reveals a complex interaction between necroptosis, tumor progression, and the immune response in CC. The findings propose a nuanced approach to leveraging necroptosis for therapeutic interventions, highlighting the potential of combining necroptosis inhibitors with existing therapies to improve treatment outcomes in CC., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)