Copper-nickel alloys can suffer severe localized corrosion in marine environments containing sulfate-reducing bacteria (SRB), but the effect of SRB on the under-deposit corrosion of copper-nickel alloys is unknown. In this work, the corrosion behavior of B10 copper-nickel alloy beneath a deposit caused by SRB with carbon source starvation in artificial seawater was studied based on electrochemical measurements and surface analysis. Results demonstrate that SRB with an organic carbon starvation can survive in artificial water but most SRB cells have died. The survived SRB cells can attach to the bare and deposit-covered B10 copper-nickel alloy, leading to the corrosion acceleration. Due to the limitation of organic carbon source, the pitting corrosion of B10 copper-nickel alloy caused by SRB is not serious. However, serious pitting corrosion of the deposit-covered B10 copper-nickel alloy can be found both in abiotic and biotic conditions, and the pitting corrosion and uniform corrosion are further accelerated by SRB. There is a galvanic effect between the bare and deposit-covered specimens in the presence of SRB in the early stage but the galvanic effect after 5 d of testing can be neglected due to the low OCP difference values.
Menglong Zhao,Danqing Wu,Weiqian Qiu,Hongchen Zhang,Min Chen,Haixia Zhou,Xiaoxia Ye,Zhong Han,Xiangchao Shi
4-anilinoquinazoline scaffold, a key structure in the development of EGFR-TKI anticancer drugs such as Gefitinib and Erlotinib, continues to drive advancements in non-small cell lung cancer (NSCLC) therapy. In this study, we synthesized a series of novel derivatives ( B3–B11 ). Structure-activity relationship (SAR) analysis revealed that electron-donating groups para-substituted at the 4-anilino position significantly enhanced antiproliferative activity. Notably, B10 incorporating an acrylamide group at the 4-anilino position demonstrated the most potent activity against NSCLC, with an IC 50 of 1.28 μM in A549 cells, nearly six times more effective than Gefitinib (7.81 μM). Acute toxicity studies confirmed that B10 is safe at doses below 50 mg/kg. In vivo studies using an A549 xenograft model showed a 46 % tumor growth inhibition (TGI) with B10 (25 mg/kg), surpassing the 21 % inhibition of Gefitinib at the same dose. Mechanistic studies revealed that B10 inhibited the AKT/GSK-3β/β-catenin signaling pathway, downregulating Wnt target genes (c-Myc, c-Jun), and reduced COX2 expression and IL-8 levels, showcasing its dual anti-inflammatory and antitumor effects. These results position B10 as a promising NSCLC therapeutic candidate, combining potent efficacy with a favorable safety profile, and enhance our understanding of the SAR and mechanism of action of 4-anilinoquinazoline derivatives.